Database Query Results : Phenethyl isothiocyanate, ,

PEITC, Phenethyl isothiocyanate: Click to Expand ⟱
Features:
Phenethyl isothiocyanate (PEITC) is a naturally occurring small-molecule phytochemical best known for its role in cancer chemoprevention research. It belongs to the isothiocyanate class of organosulfur compounds and has the chemical formula C₉H₉NS.
Source: Derived from glucosinolates in cruciferous vegetables
PEITC in plants exists mainly as the glucosinolate precursor (gluconasturtiin). Upon tissue disruption (chewing, chopping), myrosinase converts gluconasturtiin → PEITC. 
-PEITC bioavailability from fresh, chopped microgreens is high
-Co-consumption with other isothiocyanates is additive/synergistic
-Peak plasma levels: ~1–3 hours post-consumption
-Half-life: ~4–6 hours
-Generally well tolerated up to 40 mg/day (mild GI irritation at higher dose)

PEITC is best characterized for its dual role in xenobiotic metabolism:
Inhibition of Phase I enzymes
-Suppresses cytochrome P450 enzymes (e.g., CYP1A1, CYP2E1)
-Reduces activation of pro-carcinogens

-Selectively depletes GSH in cancer cells
-Directly increases ROS beyond buffering capacity

Key pathways in cancer cells
-GSH depletion
-Mitochondrial ROS amplification
-ASK1/JNK apoptosis

Chemo relevance
-Frequently chemo-sensitizing
-Opposite of NAC/GSH

Induction of Phase II enzymes
-Activates NRF2–KEAP1 signaling
-Increases expression of detoxification and antioxidant enzymes such as:
 -Glutathione S-transferases (GSTs)
 -NAD(P)H quinone oxidoreductase 1 (NQO1)
 -Heme oxygenase-1 (HMOX1)

In preclinical systems, PEITC has been shown to:
-Deplete intracellular glutathione (GSH), increasing oxidative stress in cancer cells
-Induce mitochondrial dysfunction and apoptosis
-Inhibit histone deacetylases (HDACs) (context-dependent)
-Suppress pro-survival signaling pathways (e.g., STAT3, NF-κB)
-Target cancer stem–like cells in some models

Dietary origins

PEITC present in vegetables such as:
-Watercress (the richest source)
-Broccoli
-Cabbage
-Brussels sprouts
-Radish

Bioavailability depends on:
-Food preparation
-Gut microbiota (myrosinase activity if plant enzyme is inactive)

watercress microgreens generally have higher PEITC (and/or its precursor gluconasturtiin) per gram than mature watercress.
-The enrichment is most pronounced per unit fresh weight in the 7–14 day window.
-Absolute values vary substantially with cultivar, light intensity, sulfur/nitrogen nutrition, and post-harvest handling.
| Growth stage    |      Age | PEITC potential (mg / 100 g FW) |         Relative |
| --------------- | -------: | ------------------------------: | ---------------: |
| **Microgreens** |   7–10 d |                     **3.0–6.0** | **~2–4×** mature |
| **Microgreens** |  11–14 d |                     **2.5–5.0** |            ~2–3× |
| Baby leaf       |  21–28 d |                         1.5–3.0 |            ~1–2× |
| Mature leaf     | 35–45+ d |                         0.8–1.5 |         baseline |

Dry weight basis
| Growth stage          | PEITC potential (mg / g DW) |
| --------------------- | --------------------------: |
| Microgreens (7–10 d)  |                 **1.8–3.5** |
| Microgreens (11–14 d) |                     1.5–3.0 |
| Mature leaf           |                     0.6–1.2 |

Expect 2–5× variability depending on:
-Light spectrum (blue light ↑ glucosinolates)
-Sulfur availability

Practical optimization tips
Lighting
-12–16 h/day
-150–300 µmol/m²/s PAR (typical shop LEDs at 20–30 cm distance)
Soil
-Peat or peat-blend preferred
-Avoid over-watering (dilutes concentration)
Nutrition (optional but effective)
-One light watering with ¼-strength sulfate-containing fertilizer around day 4–5 can increase PEITC ~15–30%
Harvest & use
-Cut, rest 5–10 minutes, then consume (allows myrosinase to fully convert gluconasturtiin → PEITC)

Dose: (100 g fresh microgreens ≈ 2–4 mg bioavailable PEITC)
-ie below doses are not really acheivable from fresh microgreens
Minimum biologically active dose (humans): ~10–15 mg PEITC/day
Common efficacy range used in human trials: 20–40 mg/day
Upper short-term doses studied (generally tolerated): 60 mg/day
Diet-achievable with watercress microgreens: Yes, at realistic portions
These doses are chemopreventive / pathway-modulating, not cytotoxic chemotherapy.
| PEITC dose (mg/day) | Dominant biological effects                     |
| ------------------: | ----------------------------------------------- |
|         **5–10 mg** | Phase II enzymes, mild NRF2                     |
|        **10–20 mg** | HDAC inhibition, ROS signaling                  |
|        **20–40 mg** | Apoptosis, cell-cycle arrest, anti-inflammatory |
|        **40–60 mg** | Strong redox stress in cancer cells             |
|              >60 mg | Limited data; GI irritation risk                |

Rank Pathway / Target Axis Direction Primary Effect Notes / Cancer Relevance Ref
1 GSH / thiol buffering (PEITC–GSH conjugation → GSH depletion) ↓ GSH Upstream redox collapse PEITC drives a GSH-iron-ROS axis; GSH depletion is upstream of multiple death programs (ref)
2 ROS accumulation ↑ ROS Oxidative stress trigger PEITC increases intracellular ROS, which then drives mitochondrial disruption and apoptosis (ref)
3 Ferroptosis (lipid peroxidation; anti-ferroptotic machinery overwhelmed) ↑ ferroptosis Iron-dependent oxidative death Direct evidence that PEITC induces ferroptosis (alongside other death programs) via GSH-iron-ROS mechanisms (ref)
4 Mitochondrial integrity (ΔΨm; cytochrome-c release) ↓ ΔΨm / ↑ cytochrome-c release Mitochondrial dysfunction PEITC promotes ROS, decreases ΔΨm, increases cytochrome-c release in cancer cells (ref)
5 Intrinsic apoptosis (caspase-9 → caspase-3) ↑ caspase activation / ↑ apoptosis Execution-phase cell death PEITC activates caspase-9 and caspase-3 and induces apoptosis downstream of mitochondrial dysfunction (ref)
6 Akt → JNK → Mcl-1 axis ↓ Akt / ↑ JNK / ↓ Mcl-1 Pro-survival signaling collapse Leukemia study: PEITC-initiated death is linked to Akt inactivation → JNK activation → Mcl-1 downregulation (ref)
7 NF-κB signaling ↓ NF-κB transcriptional activity / ↓ p65 nuclear translocation Reduced pro-survival / inflammatory transcription PEITC inhibits NF-κB activity and NF-κB–regulated genes (e.g., cyclin D1, VEGF, Bcl-xL) in prostate cancer cells (ref)
8 JAK–STAT3 signaling ↓ STAT3 activation Reduced survival / growth signaling PEITC inhibits IL-6–driven JAK–STAT3 activation in prostate cancer cells (STAT3 signaling direction shown) (ref)
9 Cell-cycle regulation ↑ G2/M arrest Proliferation blockade PEITC inhibits proliferation and induces G2/M cell-cycle arrest in prostate cancer cells (ref)
10 Autophagy program ↑ autophagy Stress response (can interact with death) PEITC induces autophagy along with ferroptosis and apoptosis in osteosarcoma cells (ref)
11 Migration / invasion (MMPs, FAK, RhoA) ↓ migration & invasion / ↓ MMPs Anti-metastatic phenotype PEITC suppresses migration/invasion and downregulates MMP-2/-7/-9 and motility regulators (FAK, RhoA) (ref)
12 In vivo anti-tumor effect ↓ tumor burden / ↑ survival (model-dependent) Demonstrated efficacy in animal model Leukemia study reports PEITC anti-leukemic activity including mechanistic signaling changes and in vivo efficacy evidence (ref)


Scientific Papers found: Click to Expand⟱
4959- PEITC,    Phenethyl isothiocyanate hampers growth and progression of HER2-positive breast and ovarian carcinoma by targeting their stem cell compartment
- in-vitro, Ovarian, NA
CSCs↓, Isothiocyanates elicit anticancer effects by targeting cancer stem cells (CSCs).
ALDH↓, We found that PEITC significantly impaired the SFE of HER2-positive human cancer cells by decreasing their ALDH-positive compartments
CSCsMark↓, The anti-CSC activity of PEITC was demonstrated by a reduced expression/activation of established cancer-stemness biomarkers
eff↑, , in combination with trastuzumab, by significantly reducing spontaneous tumor development in d16HER2 transgenic mice.

4918- PEITC,    Nutritional Sources and Anticancer Potential of Phenethyl Isothiocyanate: Molecular Mechanisms and Therapeutic Insights
- Review, Var, NA
Apoptosis↑, Its anticancer activities are mediated through several mechanisms, including the induction of apoptosis (programmed cell death), inhibition of cell proliferation, suppression of angiogenesis (formation of new blood vessels that feed tumors), and red
TumCP↓,
angioG↓,
TumMeta↓, reduction of metastasis (spread of cancer cells to new areas).
NF-kB↓, PEITC targets crucial cellular signaling pathways involved in cancer progression, notably the Nuclear Factor kappa-light-chain-enhancer of activated B cells (NF-κB), Protein Kinase B (Akt), and Mitogen-Activated Protein Kinase (MAPK) pathways.
Akt↓,
MAPK↓,
*BioAv↓, Isothiocyanates, including PEITC, are thermally labile, meaning they are susceptible to decomposition under heat;
ROS↑, Several studies proved that PEITC could initiate oxidative damage in the mitochondria by increasing the intracellular ROS to a highly toxic level
lipid-P↑, PEITC-induced ROS can cause lipid peroxidation of the mitochondrial membrane and, therefore, the loss of membrane integrity and the production of apoptosis-inducing factor (AIF) and apoptogenic cytochrome c (Cyt c)
AIF↑,
Cyt‑c↑,
DR4↑, PEITC can enhance TRAIL-induced apoptosis by upregulating DR4 and DR5 expression.
DR5↑,
TumCCA↑, Antiproliferative: Cell Cycle Arrest Induction
JAK↓, PEITC can hinder the activation of the JAK-STAT3 pathway,[112] decreasing the expression of MMP2 and MMP9.
STAT3↓,
MMP2↓,
MMP9↓,
PKCδ↓, efficacy of PEITC in inhibiting the protein kinase C (PKC)/MAPK pathway
Hif1a↓, PEITC can inhibit angiogenesis in cancer cells by suppressing the expression of HIF-1α
JNK↓, inhibiting the Akt pathway, activating Jun N-terminal kinase (JNK), and downregulating the Mcl-1
Mcl-1↓,
COX2↓, PEITC not only as a direct inhibitor of COX-2
MMP↓, 10 µm of PEITC caused ROS generation and mitochondrial depolarization, leading to the release of Cyt c and apoptosis mediated by activation of caspase-3, indicating that the mitochondrial membrane potential is compromised by ROS generation
Casp3↑,
ChemoSen↑, PEITC can synergize with cisplatin, doxorubicin, docetaxel, fludarabine, paclitaxel, gefitinib, or ionizing radiation to induce more pronounced apoptosis and growth inhibition in cancer than either agent alone
*BioAv↓, its low bioavailability impedes its clinical application as an oncologic treatment. PEITC is a lipophilic compound with poor water solubility, which hinders its dissolution and absorption in the gastrointestinal tract
Half-Life↓, Furthermore, rapid metabolism and elimination limit the systemic exposure of PEITC, reducing its efficacy against cancer cells.

4947- PEITC,    Phenethyl Isothiocyanate (PEITC) Inhibits the Growth of Human Oral Squamous Carcinoma HSC-3 Cells through G0/G1   Phase Arrest and Mitochondria-Mediated Apoptotic Cell Death
- in-vitro, Oral, HSC3
AntiCan↑, Phenethyl isothiocyanate (PEITC), an effective anticancer and chemopreventive agent, has been reported to inhibit cancer cell growth through cell-cycle arrest and induction of apoptotic events in various human cancer cells models.
chemoPv↑,
TumCG↓,
Apoptosis↑,
TumCCA↑, PEITC effectively inhibited the HSC-3 cells’ growth and caused apoptosis. PEITC induced G0/G1   phase arrest through the effects of associated protein such as p53, p21, p17, CDK2 and cyclin E,
P53↑,
P21↑,
BAX↑, triggered apoptosis through promotion of Bax and Bid expression and reduction of Bcl-2, leading to decrease the levels of mitochondrial membrane potential (ΔΨm), and followed the releases of cytochrome c, AIF and Endo G then for causing apoptosis in
BID↑,
Bcl-2↓,
MMP↓,
Cyt‑c↑,
AIF↑,
ROS↑, PEITC promoted the production of ROS (Figure 4(a)) and Ca2+ (Figure 4(c)) but decreased the levels of ΔΨm
Ca+2↑,

4948- PEITC,    Sensory acceptable equivalent doses of β-phenylethyl isothiocyanate (PEITC) induce cell cycle arrest and retard the growth of p53 mutated oral cancer in vitro and in vivo
- vitro+vivo, Oral, CAL27 - vitro+vivo, Oral, FaDu - vitro+vivo, Oral, SCC4 - vitro+vivo, Oral, SCC9
TumCD↑, In vitro, PEITC was selectively toxic to oral cancer cells (CAL-27, FaDu, SCC4, SCC 9, SCC15, SCC25 and TU138), compared to oral keratinocytes (OKF6/TERT2 and NOK/Si)
TumCG↓, In vivo, 5 and 10 mg kg−1 PEITC, equivalent to human organoleptically acceptable doses, retarded tumor growth and prolonged the survival of mice bearing p53-mutated oral cancer cells
OS↑,
ROS↑, Mechanistically, PEITC induced ROS accumulation, nuclear translocation of p53 and p21 and G1/S cell cycle arrest in vitro; increased p53 and 8-oxo-dG levels
P53↑,
P21↑,
TumCCA↑,
Ki-67↓, and decreased Ki-67 intense/mild staining ratios without TUNEL changes in vivo

4949- PEITC,    Phenethyl Isothiocyanate Exposure Promotes Oxidative Stress and Suppresses Sp1 Transcription Factor in Cancer Stem Cells
- in-vitro, Cerv, HeLa
ROS↑, Cruciferous vegetable-derived phenethyl isothiocyanate (PEITC) selectively induces reactive oxygen species (ROS), leading to apoptosis of cancer cells, but not healthy cells.
selectivity↑,
CSCs↓, PEITC treatments resulted in a reduced number of ALDHhi hCSCs in a concentration-dependent manner
Sp1/3/4↓, PEITC suppressed the cancer-associated transcription factor (Sp1) and a downstream multidrug resistance protein (P-glycoprotein)
P-gp↓,
ALDH↓, PEITC inhibits ALDH2 in the liver
GSH↓, The electrophilic property of PEITC has been shown to covalently interact with nucleophilic glutathione (GSH), leading to ROS-induction in cells
TumCP↓, Phenethyl Isothiocyanate Treatment Suppressed HeLa Cancer Stem Cells Proliferation and Increased Early Apoptosis
Apoptosis↑,

4950- PEITC,    Phenethyl isothiocyanate-induced apoptosis in PC-3 human prostate cancer cells is mediated by reactive oxygen species-dependent disruption of the mitochondrial membrane potential
- vitro+vivo, Pca, PC3
MMP↓, The PEITC-induced cell death in PC-3 cells was associated with disruption of the mitochondrial membrane potential, release of apoptogenic molecules (cytochrome c and Smac/DIABLO) from mitochondria to the cytosol and generation of reactive oxygen spe
Cyt‑c↑,
Smad1↑,
Diablo↑,
ROS↑,

4951- PEITC,    ROS accumulation by PEITC selectively kills ovarian cancer cells via UPR-mediated apoptosis
- in-vitro, Ovarian, PA1 - in-vitro, Ovarian, SKOV3
ROS↑, PEITC caused increased ROS-accumulation and inhibited proliferation selectively in ovarian cancer cells, and glutathione (GSH) depletion in SKOV-3.
TumCP↓,
GSH↓, One of the generating ROS mechanisms by PEITC is a depletion of GSH
selectivity↑, However, PEITC did not cause any effect in normal ovarian epithelial cells and peripheral blood mononuclear cells
UPR↑, PEITC Induces Unfolded Protein Response, Attenuated by NAC, in Ovarian Cancer Cells
CHOP↑, The key regulator of UPR-mediated apoptosis, CHOP/GADD153 and endoplasmic reticulum resident chaperone BiP/GRP78 were parallely up-regulated
ER Stress↑,
GRP78/BiP↑,
PERK↑, with activation of two major sensors of the UPR [PERK and ATF-6 in PA-1; PERK, and IRE1α in SKOV-3) in response to ROS accumulation induced by PEITC (5 μM)
ATF6↑,
eff↓, ROS scavenger, N-acetyl-L-cysteine (NAC), attenuated the effect of PEITC on UPR signatures (P-PERK, IRE1α, CHOP/GADD153, and BiP/GRP78)
TumCG↓, PEITC Inhibits Growth of Ovarian Cancer Cells without Inhibiting the Growth of Normal PBMC Cells
Apoptosis↑, PEITC Induces Apoptotic Cell Death in Ovarian Cancer Cell Lines
toxicity↓, IC50 value of PEITC for endothelial cells was more than 100 μM, suggesting cancer cell-specific cell death by PEITC (28). PEITC is a well-known ROS inducer in cancer cells without any potential adverse effect on normal cells (

4952- PEITC,    Cancer-preventive effect of phenethyl isothiocyanate through tumor microenvironment regulation in a colorectal cancer stem cell xenograft model
- in-vitro, CRC, HCT116
CSCs↓, PEITC reduced CSC properties, including clonogenicity and sphere formation, and expression level of pluripotent factors.

4953- PEITC,    PEITC: a natural compound effective in killing primary leukemia cells and overcoming drug resistance
- in-vitro, CLL, NA
ROS↑, Based on the recent observations that β-phenylethyl isothiocyanate (PEITC) causes significant ROS increase in cancer cells by disabling the GSH antioxidant system
GSH↓,
TumCD↓, PEITC effectively killed both F-ara-A sensitive (n=7, IC50 range: 0.5-10 µM) and resistant (n=4, IC50>50 µM,) CLL cells, with similar IC50 values of 4-8 µM.
eff↓, Antioxidant N-acetylcysteine (NAC) suppressed PEITC-induced ROS accumulation and cell death, suggesting that this compound killed CLL cells through ROS-mediated mechanism.
Mcl-1↓, PEITC treatment led to a significant decrease in MCL-1 protein without detectable change in BCL-2 protein level.
Casp3↑, PEITC induced caspase-3 activation

4954- PEITC,    Selective killing of oncogenically transformed cells through a ROS-mediated mechanism by β-phenylethyl isothiocyanate
- vitro+vivo, Ovarian, SKOV3
ROS↑, Here, we show that such abnormal increases in ROS can be exploited to selectively kill cancer cells using β-phenylethyl isothiocyanate (PEITC).
GSH↓, malignant cells highly sensitive to PEITC, which effectively disables the glutathione antioxidant system and causes severe ROS accumulation preferentially in the transformed cells due to their active ROS output
selectivity↑, Our study showed that PEITC has a superior selectivity compared to cisplatin. The ability to preferentially kill malignant cells is a promising feature of PEITC.
mtDam↑, Excessive ROS causes oxidative mitochondrial damage, inactivation of redox-sensitive molecules, and massive cell death.
TumCD↑,
OS↑, In vivo, PEITC exhibits therapeutic activity and prolongs animal survival.
eff↑, Furthermore, because PEITC has low toxicity in nonmalignant cells and exhibits anticancer selectivity superior to cisplatin,
*toxicity↓,
H2O2↑, t ROS induced by PEITC were mainly DCF-DA-reactive species such as hydrogen peroxide (H2O2) and nitric oxide (NO)
NO↑,
eff↓, 5 μM PEITC significantly increased DAF-FM fluorescence, which was reversed by the antioxidant N-acetyl-L-cysteine (NAC) but not by the H2O2-scavenging enzyme catalase
GPx↓, 500 μM PEITC inhibited GPX by approximately 50% and 90%, respectively. These concentrations could be achieved intracellularly when cells were incubated with 5–10 μM PEITC.
Dose↝, Interestingly, incubation of cells with 5–10 μM PEITC led to a depletion of cellular GSH, which is in the mM range. The explanation for this stoichiometric discrepancy is that PEITC can be concentrated in the cells. A
eff↑, combination of PEITC with curcumin was effective, suggesting that combination of PEITC with other agents may enhance anticancer activity.

4955- PEITC,    Phenethyl isothiocyanate-induced cytoskeletal changes and cell death in lung cancer cells
- in-vitro, Lung, A549 - in-vitro, Lung, H1299
TumCG↓, The observed growth-inhibitory effect of PEITC was dose-dependent, but time-dependence was observed only at higher concentrations.
α-tubulin↓, PEITC induced disassembly of actin stress fibers and degradation of tubulin which, most likely, contributed to the induction of cell death.
TumCD↑,
TumCCA↑, 24-h incubation caused G2/M cell cycle arrest, the fraction of G2/M cells decreased in a dose- and time-dependent manner in favor of cells with sub-G1 DNA content
Apoptosis↑, apoptosis-inducing potency of PEITC is probably the main factor responsible for cell growth inhibition.

4956- PEITC,    Inhibition of cancer growth in vitro and in vivo by a novel ROS-modulating agent with ability to eliminate stem-like cancer cells
- vitro+vivo, Lung, A549
GSH↓, synthetic analog of PEITC with superior in vitro and in vivo antitumor effects. Mechanistic study showed that LBL21 induced a rapid depletion of intracellular glutathione (GSH), leading to abnormal ROS accumulation
ROS↑,
mtDam↑, and mitochondrial dysfunction, evident by a decrease in mitochondrial respiration and transmembrane potential.
mitResp↓,
MMP↓,
CSCs↓, Importantly, LBL21 exhibited the ability to abrogate stem cell-like cancer side population (SP) cells in non-small cell lung cancer A549
OCT4↓, with a downregulation of stem cell markers including OCT4, ABCG2, SOX2 and CD133.
ABC↓,
SOX2↓,
CD133↓,
CD44↓, LBL21 caused a significant decrease in various CSC biomarkers CD44, CD133, OCT4, ABCG2, SOX2, ALDH2 and NANOG in mRNA expression levels
ALDH↓,
Nanog↓,
TumCG↓, LBL21 substantially suppressed tumor growth in A549 xenograft mice

4957- PEITC,    Phenethyl Isothiocyanate (PEITC) from Cruciferous Vegetables Targets Human Cancer Stem-Like Cells
- vitro+vivo, Cerv, HeLa
CSCs↓, PEITC attenuated proliferation of sphere-culture-enriched (ANOVA, p蠄 0.001), aldehyde dehydrogenase (ALDH1)bright, CD44high⁄+/CD24low⁄–, Hoechst 33342-excluded hCSC in a concentration- and time-dependent manner.
ALDH↓,
CD44↓,
CD24↓,
cl‑PARP↑, PEITC up-regulated cleaved poly (ADP-ribose) polymerase (p蠄 0.05) and induced death receptors, DR4 (p蠄 0.01) and DR5 (p蠄 0.001), of tumor necrotic factor-related apoptosis-inducing ligand signaling.
DR4↑,
DR5↑,

4958- PEITC,    Cancer-preventive effect of phenethyl isothiocyanate through tumor microenvironment regulation in a colorectal cancer stem cell xenograft model
- vitro+vivo, CRC, NA
CSCs↓, PEITC significantly reduced the CSC properties, including clonogenicity and the expression of pluripotent factors
TumCG↓, Prior to CSC inoculation in vivo, the PEITC pre-treatment group showed a more effective reduction in the tumor growth rate
Inflam↓, PEITC pre-treatment remarkably suppressed genes related to inflammatory and immune responses and chemokine-related signaling.

4946- PEITC,    Phenethyl Isothiocyanate Inhibits Oxidative Phosphorylation to Trigger Reactive Oxygen Species-mediated Death of Human Prostate Cancer Cells
- in-vitro, Pca, LNCaP - in-vitro, Pca, PC3
Apoptosis↑, inhibits growth of human cancer cells by causing apoptotic and autophagic cell death.
TumAuto↑,
ROS↑, we demonstrate that the PEITC-induced cell death is initiated by production of reactive oxygen species (ROS) resulting from inhibition of oxidative phosphorylation (OXPHOS)
OXPHOS↓,
ATP↓, , suppression of OXPHOS, and ATP depletion.
selectivity↑, These effects were not observed in a representative normal human prostate epithelial cell line (PrEC)
ETC↓, PEITC-induced cell death involving ROS production due to inhibition of complex III and OXPHOS.
eff↓, PEITC-mediated increase in CM· signal intensity in PC-3 cells was markedly suppressed in the presence of NAC
eff↓, Rho-0 Variants of LNCaP and PC-3 Cells Were Resistant to PEITC-induced Apoptosis
BAX↑, PEITC Treatment Caused Mitochondrial Translocation of Bax

4960- PEITC,    Phenethyl isothiocyanate upregulates death receptors 4 and 5 and inhibits proliferation in human cancer stem-like cells
- in-vivo, Cerv, HeLa
CD44↓, PEITC attenuated proliferation of CD44high/+/CD24low/–, stem-like, sphere-forming subpopulations of hCSCs in a concentration- and time-dependent manner that was comparable to the CSC antagonist salinomycin
CD24↓,
CSCs↓,
cl‑PARP↑, PEITC exposure-associated up-regulation of cPARP (apoptosis-associated cleaved poly [ADP-ribose] polymerase) levels and induction of DR4 and DR5 (death receptor 4 and 5) of TRAIL signaling were observed.
DR4↑,
DR5↑,
TumCP↓, PEITC also significantly reduced proliferation of both HeLa cells and hCSCs in a concentration-dependent manner after 24- and 48-hour exposures, which was a pattern comparable to the effects of salinomycin.

4961- PEITC,    Phenethyl isothiocyanate suppresses cancer stem cell properties in vitro and in a xenograft model
- vitro+vivo, CRC, HCT116
CSCs↓, PEITC suppressed the self-renewal capacity and clonogenicity in the EpCAM-expressing CSC model.
TumCG↓, PEITC markedly suppressed both tumor growth and expression of three pluripotency factors in a mouse xenograft model.
CSCsMark↓, CSC markers are downregulated by PEITC treatment

4962- PEITC,  Ba,  PSO,    Targeting Breast Cancer Stem Cells
- Review, BC, NA
CSCs↓, Natural compounds targeting BCSCs

4963- PEITC,    Sensory Acceptable Equivalent Doses of β - Phenylethyl isothiocyanate (PEITC) Induce Cell Cycle Arrest and Retard Growth of p53 Mutated Oral Cancer In Vitro and In Vivo
- vitro+vivo, Oral, CAL27 - vitro+vivo, Oral, FaDu - vitro+vivo, Oral, SCC4 - vitro+vivo, Oral, SCC9
Dose↝, High doses of β - Phenethyl isothiocyanate (PEITC), a phytochemical in cruciferous vegetables are not feasible for consumption due to a strong mouth-tingling effect. This study investigated the anti-cancer effect of PEITC at sensory acceptable doses.
selectivity↑, In vitro, PEITC was selectively toxic to oral cancer cells (CAL-27, FaDu, SCC4, SCC 9, SCC15, SCC25 and TU138), compared to oral keratinocytes (OKF6/TERT2 and NOK/Si).
TumCG↓, In vivo, 5 and 10 mg/kg PEITC, equivalent to human organoleptic acceptable doses, retarded tumor growth and prolonged survival of mice bearing p53-mutated oral cancer cell - TU138 xenograft.
OS↑,
ROS↑, Mechanistically, PEITC induced ROS accumulation, nuclear translocation of p53 and p21 and G1/S cell cycle arrest in vitro; increased p53 and 8-oxo-dG levels, and decreased Ki-67 intense/mild staining ratios without TUNEL changes in vivo.
P53↑,
P21↑,
TumCCA↑,
Ki-67↓,

4964- PEITC,    Irreversible Inhibition of Glutathione S-Transferase by Phenethyl Isothiocyanate (PEITC), a Dietary Cancer Chemopreventive Phytochemical
- in-vitro, Var, NA
GSH↓, . The primary route of isothiocyanate metabolism is its conjugation with glutathione (GSH), a reaction catalyzed by glutathione S-transferase (GST).
GSTA1↓,
chemoPv↑, a Dietary Cancer Chemopreventive Phytochemical

5014- PEITC,  Xan,    Combination of xanthohumol and phenethyl isothiocyanate inhibits NF-κB and activates Nrf2 in pancreatic cancer cells
- in-vitro, PC, NA
NF-kB↓, Combination of XAN and PEITC diminish activation and expression of NF-κB
NRF2↑, XAN and PEITC enhance activation and expression of Nrf2 and GSTP, NQO1, SOD.
GSTP1/GSTπ↑,
NQO1↑,
SOD↑,
TumCP↓, Treatment with these phytochemicals reduces the cancer cells proliferation.

5016- PEITC,    Phenethyl Isothiocyanate (PEITC) interaction with Keap1 activates the Nrf2 pathway and inhibits lipid accumulation in adipocytes
- in-vitro, Nor, NA
*NRF2↑, Phenethyl Isothiocyanate (PEITC) interaction with Keap1 activates the Nrf2 pathway and inhibits lipid accumulation in adipocytes
*Diff↓, PEITC was found to activate Nrf2-mediated gene expression and inhibit adipocyte differentiation, at least partially, through Nrf2-dependent mechanisms.
*Weight↓, Administration of PEITC in high-calorie diet-fed mice reduced body weight, epididymal fat weight, and hepatic lipid contents
*lipid-P↓,

5072- PEITC,    Inhibition and Inactivation of Human Cytochrome P450 Isoforms by Phenethyl Isothiocyanate
- in-vitro, Nor, NA
*CYP2E1↓, Furthermore, PEITC is a mechanism-based inactivator of human CYP2E1.
*chemoPv↑, The present study directly proved that the chemopreventive effects of PEITC for nitrosamine-induced carcinogenesis are due to the inhibition of CYP by an in vitro study.

5183- PEITC,  Cisplatin,    Phenethyl Isothiocyanate Induces Apoptosis Through ROS Generation and Caspase-3 Activation in Cervical Cancer Cells
- in-vitro, Cerv, HeLa - in-vitro, Nor, HaCaT
DNAdam↑, Phenethyl isothiocyanate alone was sufficient to cause nucleus condensation and fragmentation and induce apoptosis in cervical cancer cells, but evident synergistic effects were observed in combination with cisplatin
Apoptosis↑,
ChemoSen↑, Phenethyl Isothiocyanate Exerted Synergistic Effects With Cisplatin on CaSki Cells
ROS↑, phenethyl isothiocyanate treatment increased the production of intracellular ROS in a dose-dependent manner in cervical cancer cells.
mt-ROS↑, phenethyl isothiocyanate induced mitochondrial reactive oxygen species production, and activation of caspases showed that phenethyl isothiocyanate significantly activated caspase-3.
Casp↑,
Casp3↑,
selectivity↑, As the findings show, exposure of phenethyl isothiocyanate resulted in negligible toxicity to normal cells (HaCaT) up to a dose of 30 μM for 24 h
TumCP↓, Phenethyl Isothiocyanate Attenuated Cervical Cancer Cell Proliferation
tumCV↓, decreased the cervical cancer cell viability
eff↓, OS inhibitor N-acetylcysteine (NAC) on phenethyl isothiocyanate–mediated cytotoxic effects over CaSki and HeLa cells,

5184- PEITC,    Phenethyl isothiocyanate exhibits antileukemic activity in vitro and in vivo by inactivation of Akt and activation of JNK pathways
- vitro+vivo, AML, U937
Casp3↑, Exposure of cells to PEITC resulted in pronounced increase in the activation of caspase-3, -8, -9, cleavage/degradation of PARP, and apoptosis in dose- and time-dependent manners.
Casp9↑,
Casp8↑,
cl‑PARP↑,
Apoptosis↑,
Mcl-1↓, These events were accompanied by the caspase-independent downregulation of Mcl-1, inactivation of Akt, as well as activation of Jun N-terminal kinase (JNK)
Akt↓,
JNK↑,
eff↑, inhibition of PI3K/Akt by LY294002 significantly enhanced PEITC-induced apoptosis.

5185- PEITC,  SFN,    Suppression of NF-kappaB and NF-kappaB-regulated gene expression by sulforaphane and PEITC through IkappaBalpha, IKK pathway in human prostate cancer PC-3 cells
- in-vitro, Pca, PC3
NF-kB↓, treatment with SFN (20 and 30 microM) and PEITC (5 and 7.5 microM) significantly inhibited NF-kappaB transcriptional activity, nuclear transloction of p65, and gene expression of NF-kappaB-regulated VEGF, cylcin D1, and Bcl-X(L) in PC-3 C4 cells.
p65↓,
VEGF↓,
cycD1/CCND1↓,
Bcl-xL↓,
IKKα↓, mainly mediated through the inhibition of IKK phosphorylation, particularly IKKbeta

5186- PEITC,    Phenethyl Isothiocyanate inhibits STAT3 activation in prostate cancer cells
- in-vitro, Pca, DU145 - in-vitro, Pca, LNCaP
TumCP↓, PEITC significantly inhibited DU145 cell proliferation in a dose-dependent manner and induced the cell arrest at G2-M phase.
TumCCA↑,
STAT3↓, PEITC inhibited both constitutive and interleukin 6 (IL-6)-induced STAT3 activity in DU145 cells.
p‑JAK2↓, IL-6-stimulated phosphorylation of JAK2, an STAT3 upstream kinase, was also attenuated by PEITC.
eff↓, antioxidant reagent, N-acetyl-l-cysteine (NAC) which suppresses reactive oxygen species (ROS) generation, reversed the early inhibitory effects of PEITC on cell proliferation
TumCCA↑, PEITC Inhibits cell growth and induces G2-M phase cell cycle arrest in PCa cells
AR↓, PEITC inhibits IL-6-induced AR transcriptional activity in LNCaP cells
ROS↑, consistently suggest that PEITC induced ROS at early time of its application which in turn interfered with STAT3 activation with consequent cell growth inhibition.

5187- PEITC,    Phenethyl Isothiocyanate Inhibits Migration and Invasion of Human Gastric Cancer AGS Cells through Suppressing MAPK and NF-κB Signal Pathways
- in-vitro, GC, AGS
TumMeta↓, PEITC can inhibit migration and invasion through the extracellular signal-regulated kinases 1/2 (ERK1/2), protein kinase C (PKC) and nuclear factor-kappaB (NF-κB) signaling pathways in human gastric cells.
ERK↓, PEITC exerted an inhibitory effect on the ERK1/2, mitogen-activated protein kinase kinase 7 (MKK7)
MKK7↓,
PKCδ↓, PKC, Ras homolog gene family, member A (Rho A) and urokinase-type plasminogen activator (uPA), causing the inhibition of matrix metallopeptidase-2 (MMP-2) and -9
Rho↓,
uPA↓,
MMP2↓,
MMP9↓,
RAS↓, PEITC also inhibited Ras, growth factor receptor-bound protein 2 (GRB2), vascular endothelial growth factor (VEGF), focal adhesion kinase (FAK), inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), causing inhibition of cell prolifera
VEGF↓,
FAK↓,
iNOS↓,
COX2↓,
TumCP↓,

4931- PEITC,    Phenethyl isothiocyanate (PEITC) suppresses prostate cancer cell invasion epigenetically through regulating microRNA-194
- in-vitro, Pca, LNCaP - in-vitro, Pca, PC3
Risk↓, The glucosinolate-derived PEITC has been widely documented to reduce the risk of prostate cancer by modulating multiple biologically relevant processes.
miR-194↑, PEITC treatment decreased miR-106a/b and miR-695 levels in LNCaP cells (Fig 1B), whereas miR-194 levels were up-regulated in both the LNCaP and the PC3 cells
TumCI↓, miR-194 suppresses PC3 cell invasiveness in vitro
MMP2↓, PEITC down-regulates MMP2 and MMP9 via miR-194
MMP9↓,
BMP2↓, We found that both miR-194 mimic and PEITC treatments decreased BMP1 expression
*chemoPv↑, In addition, growing evidence has suggested that epigenetic mechanisms, particularly those mediated by miRNAs, are implicated in the chemopreventive effects of PEITC

4919- PEITC,    Natural compound PEITC inhibits gain of function of p53 mutants in cancer cells by switching YAP-binding partners between p53 and p73
- in-vitro, Var, NA
Apoptosis↑, anticancer activities by modulating apoptosis, cell cycle arrest, drug-metabolizing enzymes and even preferentially restoring a ‘WT-like’ conformation to p53
TumCCA↑,
P53↓,

4920- PEITC,  Cisplatin,    PEITC restores chemosensitivity in cisplatin-resistant non-small cell lung cancer by targeting c-Myc/miR-424-5p
- vitro+vivo, NSCLC, A549
TumCG↓, PEITC inhibited the growth and increased the sensitivity of cisplatin-resistant NSCLC cells by targeting c-Myc and down-regulating the PI3K/AKT/mTOR pathway.
ChemoSen↑,
cMyc↓, this compound led to down-regulation of miR-424-5p and c-Myc
PI3K↓,
Akt↓,
mTOR↓,
BioAv↝, Cutting or chewing a cruciferous vegetable activates the release of ITCs, but heating these vegetables deactivates the enzyme
tumCV↓, gradual decrease in cell viability with increasing PEITC concentration in both NSCLC cisplatin resistance cell lines
ChemoSen↑, each drug can be reduced in combination to achieve the same effect as a single agent.

4921- PEITC,    The Potential Use of Phenethyl Isothiocyanate for Cancer Prevention
- Review, Var, NA
antiOx↑, PEITC are antioxidant, anti-inflammatory, and anti-cancer
Inflam↓,
AntiCan↑,
TumCP↓, PEITC was also predicted to reduce the expression of carcinogenesis, in-hibit cell proliferation, down-regulate the cell cycle, and enhance tumor suppression via apoptosis and autophagy induction.
TumCCA↑,
Apoptosis↑,
TumAuto↑,
HDAC↓, isothiocyanate inhibits histone dea-cetylase (HDAC) activity in human colorectal and prostate cancercells.
Risk↓, Chemicals that have demonstrated inhibitory effects on cancer cells include capsaicin, cucurbitacin B, isoflavones, catechins, lycopenes, benzyl isothiocyanate, phenethyl isothiocyanate, and piperlongumine

4922- PEITC,    Phenethyl Isothiocyanate: A comprehensive review of anti-cancer mechanisms
- Review, Var, NA
Risk↓, strong inverse relationship between dietary intake of cruciferous vegetables and the incidence of cancer.
AntiCan↑, Phenethyl isothiocyanate (PEITC) is present as gluconasturtiin in many cruciferous vegetables with remarkable anti-cancer effects.
TumCP↓, PEITC targets multiple proteins to suppress various cancer-promoting mechanisms such as cell proliferation, progression and metastasis
TumMeta↓,
ChemoSen↑, combination of PEITC with conventional anti-cancer agents is also highly effective in improving overall efficacy
*BioAv↑, ITCs are released from glucosinolates by the action of the enzyme myrosinase. The enzyme myrosinase can be activated by cutting or chewing the vegetables, but heating can destroy its activity
*other↝, Although water cress and broccoli are known to be the richest source, PEITC can also be obtained from turnips and radish
*Dose↝, In a study conducted with human volunteers, approximately 2 to 6 mg of PEITC was found to be released by the consumption of one ounce of watercress
Dose↓, significant anti-cancer effects can be achieved at micromolar concentrations of PEITC.
*BioAv↑, PEITC is highly bioavailable after oral administration. A single dose of 10–100 μmol/kg PEITC in rats resulted in bioavailability ranging between 90–114%
*Dose↝, Furthermore, about 928.5±250nM peak plasma concentration of PEITC was achieved in human subjects, after the consumption of 100g watercress.
*Half-Life↝, time to reach peak plasma concentration was observed to be 2.6h±1.1h with a t1/2 4.9±1.1h
*toxicity↝, long term studies are required to establish the safety profile of PEITC, since regular intake of PEITC can cause its accumulation resulting in cumulative effects, which could be toxic.
GSH↓, The conjugation of PEITC with intracellular glutathione and the subsequent removal of the conjugate result in depletion of glutathione and alteration in redox homeostasis leading to oxidative stress
ROS↑, PEITC-mediated generation of reactive oxygen species (ROS) is known to be a general mechanism of action leading to cytotoxic effects, especially specific to cancer cells
CYP1A1↑, PEITC on one hand causes induction of CYP1A1 and CYP1A2; however, it inhibits activity of certain CytP450 enzymes, such as CYP2E1, CYP3A4 and CYP2A3
CYP1A2↑,
P450↓,
CYP2E1↑,
CYP3A4↓,
CYP2A3/CYP2A6↓,
*ROS↓, PEITC treatment caused a significant increase in the activities of ROS detoxifying enzymes such as glutathione peroxidase1, superoxide dismutase 1 and 2. This was also confirmed in human study where subjects were administered watercress, a major sour
*GPx1↑,
*SOD1↑,
*SOD2↑,
Akt↓, PEITC inhibits Akt, a component of Ras signaling to inhibit tumor growth in several cancer types
EGFR↓, PEITC is also known to inhibit EGFR and HER2, which are important growth factors and regulators of Akt in different cancer models
HER2/EBBR2↓,
P53↑, PEITC-mediated activation of another tumor suppressor, p53 was observed in oral squamous cell carcinoma, causing G0/G1 phase arrest in multiple myeloma,
Telomerase↓, PEITC has been shown to inhibit telomerase activity in prostate and cervical cancer cells
selectivity↑, generation of reactive oxygen species (ROS), which also has been shown to be the basis of selectivity of PEITC toward cancer cells leaving normal cells undamaged [
MMP↓, ROS generation by PEITC leads to mitochondrial deregulation and modulation of proteins like Bcl2, BID, BIM and BAX, causing the release of cytochrome c into cytosol leading to apoptosis
Cyt‑c↑,
Apoptosis↑,
DR4↑, induction of death receptors and Fas-mediated apoptosis
Fas↑,
XIAP↓, PEITC-mediated suppression of anti-apoptotic proteins like XIAP and survivin, which are up-regulated in cancer cells
survivin↓,
TumAuto↑, PEITC induces autophagic cell death in cancer cells
Hif1a↓, PEITC directly or indirectly suppresses HIF1α
angioG↓, is possible that PEITC can block angiogenesis by non-hypoxic mechanisms also.
MMPs↓, Various studies with PEITC have shown suppression of invasion through inhibition of matrix metalloproteinases along with anti-metastatic effects caused by suppression of ERK kinase activity and transcriptional activity of NFkB
ERK↓,
NF-kB↓,
EMT↓, PEITC was also known to inhibit processes, such as epithelial to mesenchymal transition (EMT), cell invasion and migration, which are essential pre-requisites for metastasis
TumCI↓,
TumCMig↓,
Glycolysis↓, reduced rates of glycolysis in PEITC-treated cells and depletion of ATP lead to death in prostate cancer cells
ATP↓,
selectivity↑, PEITC (5μM) treatment suppressed glycolysis in the cancer cells, but no changes were observed in normal cells.
*antiOx↑, the antioxidant effect is achieved at very low ITC levels in normal cells as shown in various animal models
Dose↝, At higher concentrations, ITCs may generate ROS by depleting antioxidant levels. PEITC is known to cause ROS generation, which is the major mechanism of toxicity in cancer cells
other↝, There is a continuous leakage of electrons from the electron transport chain (ETC), which is major source of ROS production. PEITC causes generation of endogenous ROS by disrupting mitochondrial respiratory chain
OCR↓, PEITC also inhibits mitochondrial complex III activity and reduces the oxygen consumption rate in prostate cancer cells
GSH↓, PEITC binds to GSH and causes its depletion in cancer cells leading to ROS-induced cell damage
ITGB1↓, PEITC was found to inhibit major integrins, such as ITGB1, ITGA2 and ITGA6 in prostate cancer cells
ITGB6↓,
ChemoSen↑, Using pre-clinical studies, improved outcomes were observed when the conventional agents, such as docetaxel, metformin, vinblastine, doxorubicin and HDAC inhibitors were combined with PEITC

4923- PEITC,    Quantitative chemical proteomics reveals that phenethyl isothiocyanate covalently targets BID to promote apoptosis
- Study, Var, NA
cl‑BID↑, We show that BID, an apoptosis regulator of the Bcl-2 family, is covalently modified by ITCs on its N-terminal cysteines. PEITC promotes the cleavage and mitochondrial translocation of BID
Apoptosis↑, leading to a strong induction of apoptosis.
Bcl-xL↓, this exposure allows BID to bind anti-apoptotic proteins such as Bcl-xL, thereby suppressing their anti-apoptotic activity.
Casp8↑, Meanwhile, caspase-8 is activated shortly after PEITC treatment [12], leading to the cleavage of PEITC-modified full-length BID.
Cyt‑c↑, induce cytochrome c release

4924- PEITC,    Nutri-PEITC Jelly Significantly Improves Progression-Free Survival and Quality of Life in Patients with Advanced Oral and Oropharyngeal Cancer: A Blinded Randomized Placebo-Controlled Trial
- Trial, Oral, NA
QoL↑, higher proportion of participants with improved HRQOL, stable disease, and increased serum p53 levels
P53↑,
OS↑, The PFS time in the study group was significantly longer than that of the control group (p < 0.05).
Cyt‑c↝, Serum cytochrome c levels were non-significantly decreased in the study group
other↝, β-phenylethyl isothiocyanate (PEITC) is a phytochemical naturally present in cruciferous vegetables such as watercress, broccoli, wasabi, and cabbage
ROS↑, PEITC was selectively toxic to numerous types of cancer cells via reactive oxygen species, (ROS)-mediated mechanisms
selectivity↑,
P21↑, PEITC led to increased oxidative stress, nuclear translocation of p53 and p21, and cell cycle arrest in TP53-mutated oral cancer cells
TumCCA↑,
Dose↝, PEITC at 5 or 10 mg per kg body weight can slow down tumor growth and prolong the survival of cancer-bearing mice along with increased p53 expression
BioAv↑, Nutri-PEITC Jelly containing 40 mg of PEITC per day can be absorbed rapidly within a few hours and eliminated completely within 24 h
Weight↑, the Nutri-PEITC Jelly group had a significantly higher proportion of participants with improved BMI than that of the placebo control group (40% vs. 20%, p < 0.05)
chemoP↑, Therefore, Nutri-PEITC Jelly at the dose of 20 mg/day of PEITC did not inhibit the disease progression and the clinical application of this product is rather a functional food for tertiary chemoprevention than a therapy.

4925- PEITC,    PEITC triggers multiple forms of cell death by GSH-iron-ROS regulation in K7M2 murine osteosarcoma cells
- in-vitro, OS, NA
tumCV↓, PEITC dose-dependently inhibited the viability of K7M2 murine osteosarcoma cells with an IC50 value of 33.49 μM at 24 h.
TumCP↓, PEITC (1, 15, 30 μM) dose-dependently inhibited the cell proliferation, caused G2/M cell cycle arrest, depleted glutathione (GSH), generated reactive oxygen species (ROS)
TumCCA↑,
GSH↓,
ROS↑,
Ferroptosis↑, altered iron metabolism, and triggered multiple forms of cell death, namely ferroptosis, apoptosis, and autophagy in K7M2 cells.
Apoptosis↑,
TumAuto↑,
MAPK↑, PEITC treatment activated MAPK signaling pathway, and ROS generation was a major cause of PEITC-induced cell death.
TumCG↓, osteosarcoma mouse model, administration of PEITC (30, 60 mg/kg every day, ig, for 24 days) significantly inhibited the tumor growth
Dose⇅, but higher dose of PEITC (90 mg/kg every day) compromised its anti-osteosarcoma effect.

4926- PEITC,    PEITC inhibits the invasion and migration of colorectal cancer cells by blocking TGF-β-induced EMT
- in-vitro, CRC, SW48
TumCI↓, PEITC inhibits the invasion and migration of colorectal cancer cells.
TumCMig↓,
EMT↓, PEITC suppresses the EMT of colorectal cancer cells
Smad1↓, PEITC blocks the TGF-β1/Smad signaling pathway and TGF-β1 induced EMT.
AntiCan↑, PEITC exerts remarkable anti-cancer effects in several types of cancer, such as gastric cancer [20], lung cancer [21], prostate cancer [22], melanoma [23], breast cancer [24] and CRC
Snail↓, (SNAIL1, SLUG, ZEB1 and ZEB2). As shown in the Fig. 3B, PEITC treatment downregulated the expression levels of these four genes
Slug↓,
Zeb1↓,
ZEB2↓,
TGF-β1↓, PEITC significantly decreased the levels of TGF-β1 in SW480 cells.
eff↑, A recent study demonstrated the chemopreventive role of PEITC and curcumin in prostate cancer xenografts
E-cadherin↑, PEITC was found to upregulate epithelial markers (E-cadherin) and downregulate mesenchymal markers (N-cadherin, Vimentin) of CRC cells.
N-cadherin↓,
Vim↓,

4927- PEITC,    Targeting ferroptosis in osteosarcoma
- Review, OS, NA
AntiCan↑, β-Phenethyl isothiocyanate (PEITC) is widely found in cruciferous vegetables and has anti-cancer potential
BioAv↑, great value in OS treatment owing to its unique biological properties such as low clearance and high bioavailability
Ferroptosis↑, mechanism of action is thought to be linked to ferroptosis
TfR1/CD71↑, uplifting the expression of transferrin receptor 1 (TfR1) and elevating the level of reactive iron.
Iron↑,
ROS↑, PEITC induced oxidative stress. Malondialdehyde (MDA) and ROS, products of lipid peroxidation, were raised and GPX4 was diminished to impair intracellular antioxidant defence systems
MDA↑,
lipid-P↑,
GPx4↓,

4928- PEITC,    Dietary phytochemical PEITC restricts tumor development via modulation of epigenetic writers and erasers
- vitro+vivo, Colon, SW-620
Risk↓, Dietary intake of bioactive phytochemicals including the cruciferous vegetable derivative phenethyl isothiocyanate (PEITC) can reduce risk of human cancers, but possible epigenetic mechanisms of these effects are yet unknown.
HDAC↓, Sustained PEITC exposure not only blocked HDAC binding to euchromatin but was also associated with hypomethylation of PcG target genes that are typically hypermethylated in cancer.
TumW↓, The mean weight of tumors generated by SW620-PEITC cells was 63.6% of that generated by SW620-CON cells assessed at the same time point
TumCG↓, indicating that long-term exposure to low concentration of PEITC can potently restrict tumor growth in vivo.
AP-1↓, Unlike SW620-CON cells, tumor cells treated with PEITC displayed impaired signaling via AP-1 (activator protein 1), CRE/CREB (cAMP response elements), and NFkB pathways (Fig. 4c).
cAMP↓,
NF-kB↓,
BMI1↓, substantial down-regulation of PcG complex proteins including BMI-1 (B cell-specific Moloney murine leukemia virus integration site 1), SUZ12 (suppressor of zeste 12 homolog), EZH2 (enhancer of zeste homolog 2), Ring1A, and Ring1B.
SUZ12↓,
EZH2↓,
selectivity↑, ntriguingly, this PEITC-induced decrease in expression of PcG complex proteins was more pronounced in metastatic SW620 cells than in non-metastatic SW480 cells.

4929- PEITC,  PacT,    Phenethyl isothiocyanate and paclitaxel synergistically enhanced apoptosis and alpha-tubulin hyperacetylation in breast cancer cells
- in-vitro, BC, MCF-7 - in-vitro, BC, MDA-MB-231
ChemoSen↑, Combination of phenethyl isothiocyanate (PEITC) and paclitaxel (taxol) has been shown to work synergistically to increase apoptosis and cell cycle arrest in breast cancer cells.
Apoptosis↑,
TumCCA↑,
eff↑, treatment of MCF7 cells with both PEITC and taxol led to a 10.4-fold and 5.96-fold increase in specific acetylation of alpha-tubulin over single agent PEITC and taxol, respectively.
CDK1↓, The combination of PEITC and taxol also reduced expressions of cell cycle regulator Cdk1, and anti-apoptotic protein bcl-2, enhanced expression of Bax and cleavage of PARP proteins.
Bcl-2↓,
BAX↑,
cl‑PARP↑,
SAL↑, PEITC and taxol increased acetylation of alpha-tubulin in breast cancer cells. 16% and 28% respective increase in the specific acetylation level (SAL)

4930- PEITC,    Targeted anti-cancer therapy: Co-delivery of VEGF siRNA and Phenethyl isothiocyanate (PEITC) via cRGD-modified lipid nanoparticles for enhanced anti-angiogenic efficacy
- vitro+vivo, Lung, A549
VEGF↓, The co-delivery of VEGF siRNA and PEITC could achieve precise silencing of VEGF, inhibit the accumulation of HIF-1α under hypoxic conditions, and induce apoptosis in tumor cells.
Hif1a↓,
TumCG↓, CS-siRNA/PEITC&L-cRGD NPs possess efficient anti-tumor ability and can effectively inhibit tumor growth and proliferation.
TumCP↓,

4945- PEITC,    Phenethyl isothiocyanate (PEITC) promotes G2/M phase arrest via p53 expression and induces apoptosis through caspase- and mitochondria-dependent signaling pathways in human prostate cancer DU 145 cells
- in-vitro, Pca, DU145
AntiCan↑, Phenethyl isothiocyanate (PEITC), one of many compounds found in cruciferous vegetables, has been reported as a potential anticancer agent.
TumCG↓, PEITC was shown to inhibit cell growth and induction of apoptosis in many cancer cell lines.
Apoptosis↑,
tumCV↓, PEITC induced a dose-dependent decrease in cell viability through induction of cell apoptosis and cell cycle arrest in the G(2)/M phase of DU 145 cells.
TumCCA↑,
DNAdam↑, PEITC induced morphological changes and DNA damage in DU 145 cells.
P53↑, was mediated by the increase of p53 and WEE1 and it reduced the level of CDC25C protein.
CDC25↓,
Casp9↑, The induction of apoptosis was mediated by the activation of caspase-8-, caspase-9- and caspase-3-depedent pathways.
Casp8↑,
mtDam↑, PEITC caused mitochondrial dysfunction, increasing the release of cytochrome c and Endo G from mitochondria, and led cell apoptosis through a mitochondria-dependent signaling pathway.
Cyt‑c↑,

4932- PEITC,    Pharmacokinetics and Pharmacodynamics of Phenethyl Isothiocyanate: Implications in Breast Cancer Prevention
- Review, BC, NA
TumCCA↑, pharmacodynamics of PEITC in breast cancer that include cancer cell apoptosis by upregulation of apoptotic genes, cell cycle arrest at G2/M phase by generation of reactive oxygen species and depletion of intracellular glutathione
ROS↑,
GSH↓,
ERα/ESR1↓, downregulation of the estrogen receptor, decrease in sensitivity to estrogen, and inhibition of tumor metastasis.
TumMeta↓,
angioG↓, Inhibition of angiogenesis is one of the recently reported mechanisms of breast cancer prevention by PEITC.

4933- PEITC,    Phenethyl isothiocyanate inhibits metastasis potential of non-small cell lung cancer cells through FTO mediated TLE1 m6A modification
- vitro+vivo, Lung, H1299 - vitro+vivo, SCC, H226
AntiCan↓, Isothiocyanates (ITCs) are natural compounds and inhibit the tumorigenesis of various cancers.
TumCP↓, Our previous studies show that ITCs inhibit the proliferation and metastasis of non-small cell lung cancer (NSCLC) cells, and have synergistic effects with chemotherapy drugs
TumMeta↓,
ChemoSen↑,
tumCV↓, We showed that phenethyl isothiocyanate (PEITC) dose-dependently inhibited the cell viability of both NSCLC cell lines H1299 and H226 with IC50 values of 17.6 and 15.2 μM, respectively.
TumCI↓, Furthermore, PEITC dose-dependently inhibited the invasion and migration of H1299 and H226 cells.
TumCMig↓,
FTO↓, PEITC treatment dose-dependently increased m6A methylation levels and inhibited the expression of the m6A demethylase fat mass and obesity-associated protein (FTO) in H1299 and H226 cells
TLE1↓, Moreover, we showed that PEITC suppressed the migration of NSCLC cells by inhibiting TLE1 expression and downstream Akt/NF-κB pathway.
Akt↓,
NF-kB↓,

4934- PEITC,    Differential induction of apoptosis in human breast cancer cell lines by phenethyl isothiocyanate, a glutathione depleting agent
- in-vitro, BC, MCF-7 - in-vitro, BC, MDA-MB-231
GSH↓, Phenethyl isothiocyanate (PEITC) is a naturally occurring electrophile which depletes intracellular glutathione (GSH) levels and triggers accumulation of reactive oxygen species (ROS)
ROS↑,
chemoPv↑, PEITC is of considerable interest as a potential chemopreventive/chemotherapeutic agent
Apoptosis↑, PEITC readily induced apoptosis in MDA-MB-231 cells (associated with rapid activation of caspases 9 and 3, and decreased expression of BAX), MCF7 cells were relatively resistant to the apoptosis promoting effects of PEITC.
Casp9↑,
Casp3↑,
eff↓, pre-treatment of MDA-MB-231 cells with NAC rendered these cells relatively resistant to PEITC-induced apoptosis.
TumCG↓, PEITC-induced growth inhibition in human breast cancer cell lines
TumCCA↑, There was also an increase in the proportion of cells in S phase, and cells with sub-G1 DNA content, indicative of cell death, especially after 48 h.
BAX↑, An increase in BAX expression was observed at 2 h after addition of PEITC in MDA-MB-231 cells, and BAX levels further increased at 4 and 6 h (
Nrf1↑, PEITC increased NRF2 expression by ~3-fold in MDA-MB-231 cells at 4 h after treatment with PEITC. By contrast, NRF2 expression in MCF7 cells was not effected by PEITC
GSH↓, Total GSH and GSSG levels were reduced in MCF7 cells at 2 h after treatment with PEITC, but then remained at this level for the remainder of the time course
GSSG↓,
GSH/GSSG↓, By contrast, in MDA-MB-231 cells, total GSH levels decreased up to 6 h and were reduced by ~50% at this time. There was also an increase in the GSSG/GSH ratio, indicative of increasing oxidative stress.

4935- PEITC,    Phenethyl Isothiocyanate Suppresses Inhibitor of Apoptosis Family Protein Expression in Prostate Cancer Cells in Culture and In Vivo
- in-vivo, Pca, LNCaP - in-vivo, Pca, PC3
Apoptosis↑, Cruciferous vegetable constituent phenethyl isothiocyanate (PEITC) causes apoptosis in prostate cancer cells through mechanisms not fully understood
XIAP↓, Exposure of PC-3 and LNCaP human prostate cancer cells to PEITC resulted in downregulation of XIAP and Survivin proteins and Survivin mRNA.
survivin↓,
*BioAv↑, PEITC is generated upon cutting or chewing of cruciferous vegetables due to myrosinase-catalyzed breakdown of the gluconasturtiin
tumCV↓, PEITC-Mediated Inhibition of Cell Viability and Apoptosis Induction
eff↓, Moreover, Survivin overexpression conferred modest but significant protection against PEITC-mediated inhibition of PC-3 cell migration

4936- PEITC,    PEITC treatment suppresses myeloid derived tumor suppressor cells to inhibit breast tumor growth
- in-vivo, BC, MDA-MB-231
TumCG↓, oral administration of 12 μmol PEITC attenuated tumor growth by 76%.
CD34↓, significant reduction in the levels of MDSCs bearing the surface markers CD33, CD34 and CD11b in PEITC treated mice
CD11b↓,
CSCs↓,
ALC∅, Surprisingly, PEITC treatment had no effect on the lymphocyte population
CD4+↓, Our results revealed that PEITC treatment caused a small reduction in CD4+ lymphocytes
NF-kB↓, PEITC acts as a strong antitumor agent by inhibiting survival pathways, such as, nuclear factor kB (NFkB), signal transducer and activator of transcription 3 (STAT3) and hypoxia inducible factor 1α (HIF1α)
STAT3↓, Previous studies have shown that inhibition of these pathways suppresses MDSC activity and inhibits cancer progression
Hif1a↓,

4937- PEITC,    PEITC: Functional Compound for Primary and Tertiary Chemoprevention of Cancer
chemoPv↑, The findings highlight PEITC as a primary chemopreventive agent to prevent the initiation of carcinogenesis.
tumCV↓, Interestingly, the very same compound PEITC also shows promising effects in selectively removal of cancer cells in vitro and in vivo. T
GSH↓, The anti-cancer mechanisms are mostly mediated through glutathione conjugation and redox balance shift toward increased oxidative stress leading to cell death.
ROS↑,
*toxicity↝, it is safe at 40 mg per day in human

4938- PEITC,    Clinical Trial of 2-Phenethyl Isothiocyanate as an Inhibitor of Metabolic Activation of a Tobacco-Specific Lung Carcinogen in Cigarette Smokers
- Trial, Nor, NA
*Risk↑, PEITC as an inhibitor of lung carcinogenesis by NNK in smokers
*P450↓, Multiple studies have clearly demonstrated that the major mechanism by which PEITC inhibits carcinogenesis by NNK is inhibition of its metabolic activation by cytochrome P450 enzymes
*BioAv↑, Urinary levels of both PEITC-NAC and total isothiocyanates (ITC) were significantly elevated in the PEITC treatment periods compared with the placebo periods among all subjects by a magnitude of more than 150 times
*BioAv↑, PEITC is fat soluble. Thus, delivery of PEITC in olive oil avoids concerns about bioavailability;
*BioAv↑, urinary excretion of PEITC equivalents (measured as PEITC-NAC) averaged 13.5 mg in 24 hours in the study participants, which was approximately only one-third the amount of PEITC equivalents (36.6–37.7 mg) excreted
*Dose↝, phase I study with a daily dose of 120 mg PEITC, the maximum amount of PEITC-NAC in the urine was not reached until 2 weeks of daily dosing
Dose↝, watercress consumption is an attractive way to deliver PEITC because of the relatively high concentrations of the PEITC precursor gluconasturtiin in this vegetable, which can be consumed in a more pleasing way than the dosing form used here

4939- PEITC,    Phenethyl Isothiocyanate Inhibits Angiogenesis In vitro and Ex vivo
- in-vitro, Pca, PC3 - ex-vivo, Nor, HUVECs
Risk↓, affords significant protection against chemically induced cancer in animal models but also inhibits growth of cancer cells in culture and in vivo by causing cell cycle arrest and apoptosis induction.
angioG↓, We now report a novel response to PEITC involving inhibition of angiogenesis in vitro and ex vivo at pharmacologically achievable concentrations.
VEGF↓, PEITC treatment reduced migration by PC-3 human prostate cancer cells, which correlated with inactivation of Akt and suppression of VEGF, epidermal growth factor (EGF),
TumCMig↓,
Akt↓,
EGF↓,
TumCMig↓, PEITC treatment inhibits PC-3 cell migration.

4940- PEITC,    Phenethyl Isothiocyanate (PEITC) Inhibits the Growth of Human Oral Squamous Carcinoma HSC-3 Cells through G 0/G 1 Phase Arrest and Mitochondria-Mediated Apoptotic Cell Death
- in-vitro, Oral, HSC3
TumCCA↑, reported to inhibit cancer cell growth through cell-cycle arrest and induction of apoptotic events in various human cancer cells models
Apoptosis↑, PEITC induced cytotoxic effects on HSC-3 cells through the induction of apoptosis, and it also related to the involvement of ROS via mitochondria-dependent signal pathways.
BAX↑, it triggered apoptosis through promotion of Bax and Bid expression and reduction of Bcl-2, leading to decrease the levels of mitochondrial membrane potential (ΔΨm)
BID↑,
Bcl-2↓,
MMP↓,
Cyt‑c↑, and followed the releases of cytochrome c, AIF and Endo G then for causing apoptosis in HSC-3 cells.
AIF↑,
tumCV↓, PEITC Induced Cell-Morphological Changes and Decreased the Percentage of Viable Cells
ROS↑, We confirmed that whether PEITC-induced apoptosis is accompanied by the production of ROS and Ca2+ . PEITC promoted the production of ROS (Figure 4(a)) and Ca2+
Ca+2↑,
CDC25↓, PEITC decreased expression of cdc25A, CDK6 and cyclin D (Figure 5(a)), CDK2 and cyclin E (Figure 5(b)) proteins but increased the levels of p15
CDK6↓,
cycD1/CCND1↓,
CDK2↓,
cycE/CCNE↓,
P53↑, but increased the levels of p15 (Figure 5(a)), p53, p27, and p21 (Figure 5(b)) that led to G 0/G 1 phase arrest in HSC-3 cells.
p27↑,
P21↑,
Casp9↑, Here, we found that PEITC promoted ROS production and decreased the levels of ΔΨm and cytochrome c release, the activation of caspase-9 and caspase-3
Casp3↑,
GRP78/BiP↑, promotion of ROS and Ca2+ production that caused ER stress which based on increasing the GRP78 and ROS,

4941- PEITC,    PEITC: A resounding molecule averts metastasis in breast cancer cells in vitro by regulating PKCδ/Aurora A interplay
- in-vitro, BC, MCF-7 - in-vitro, BC, MDA-MB-231
PKCδ↑, PEITC was found to increase the expression of PKCδ with subsequent nuclear translocation
Apoptosis↓, PEITC was chaperoned with inhibition of the aggressiveness of breast cancer cells and ultimately induction of apoptosis.
selectivity↑, However, PEITC did not elicit any cytotoxic effect in normal breast epithelial cell line MCF-10A.
tumCV↓, The percentage of viable MDA-MB-231 cells was not significantly reduced at a lower concentration (1 μM) of PEITC but at highest concentration (5 μM), used
p‑NRF2↑, PEITC-mediated upregulation of PKCδ escalated Nrf2 phosphorylation at Ser 40 residue as well as nuclear accumulation of phospho-Nrf2. Total Nrf2 expression was found to be increased alongside the cytoplasmic fraction, but not in the nuclear one.
cl‑PARP1↑, PARP1 cleavage was observed in PEITC-treated MCF-7 and MDA-MB-231 cells.
TumCMig↓, PEITC restrained the migratory ability of breast cancer cells by regulating serine/threonine kinase signaling
ROS↓, Our team previously demonstrated facilitation of nuclear translocation of Nrf2 to nucleus from cytosol upon PEITC treatment which by activating diverse antioxidant enzymes reduced intracellular burden of reactive oxygen species (ROS) in breast cancer
Hif1a↓, PEITC in breast cancer cells as observed earlier in our laboratory evidenced downregulation of HIF1α due to potential activation of Nrf2 and subsequent induction of cellular antioxidant system [

4942- PEITC,    Phenethyl Isothiocyanate (PEITC) Inhibits the Growth of Human Oral Squamous Carcinoma HSC-3 Cells through G(0)/G(1) Phase Arrest and Mitochondria-Mediated Apoptotic Cell Death
- in-vitro, Oral, HSC3
chemoPv↑, Phenethyl isothiocyanate (PEITC), an effective anticancer and chemopreventive agent, has been reported to inhibit cancer cell growth through cell-cycle arrest and induction of apoptotic events in various human cancer cells models
TumCG↓,
TumCCA↑,
Apoptosis↑, PEITC effectively inhibited the HSC-3 cells' growth and caused apoptosis.
BAX↑, triggered apoptosis through promotion of Bax and Bid expression and reduction of Bcl-2, leading to decrease the levels of mitochondrial membrane potential (ΔΨm),
BID↑,
Bcl-2↓,
MMP↓,
Cyt‑c↑, and followed the releases of cytochrome c, AIF and Endo G then for causing apoptosis in HSC-3 cells
AIF↑,
ROS↑, PEITC promoted the production of ROS (Figure 4(a)) and Ca2+
Ca+2↑,

4943- PEITC,    Phenethyl isothiocyanate (PEITC) inhibits growth of ovarian cancer cells by inducing apoptosis: role of caspase and MAPK activation
- in-vitro, Ovarian, OVCAR-3
TumCD↑, PEITC was cytotoxic to OVCAR-3 cells, and inhibited proliferation in a dose-dependent fashion (IC(50) = 23.2 microM).
TumCP↓,
Apoptosis↑, PEITC induced apoptosis by activating caspase-3 and -9, without capsase-8 activation.
Casp3↑,
Casp9↑,
Bcl-2↓, Anti-apoptotic Bcl-2 levels were suppressed while pro-apoptotic Bax levels were enhanced.
BAX↑,
Akt↓, PEITC suppressed activation of Akt, ERK1/2, and the expression of transcription factor c-Myc, while simultaneously activating pro-apoptotic p38 and JNK1/2.
ERK↓,
cMyc↓,
p38↑,
JNK↑,
eff↓, Specific inhibitors of caspase-3 and -9, JNK1/2, and p38 reversed the cytotoxic effect of PEITC.

4944- PEITC,    Phenethyl isothiocyanate induces DNA damage-associated G2/M arrest and subsequent apoptosis in oral cancer cells with varying p53 mutations
- in-vitro, Oral, NA
TumCG↓, PEITC was able to inhibit cell growth, arrest G2/M phase, and induce apoptosis of OSCC cells.
TumCCA↑, PEITC-induced G2/M phase arrest and apoptosis depend on the GSH redox stress- and p53-related pathway
Apoptosis↑,
ROS↑, PEITC induced reactive oxygen species and NO production, GSH depletion, and ΔΨm reduction in OSCC cells.
NO↑,
GSH↓,
MMP↓,
DNAdam↑, PEITC-induced oxidative DNA damage was associated with the activation of the ATM–Chk2–p53 pathway.
ATM↑,
Chk2↑,
P53↑,
eff↓, Pifithrin-α, NAC, or GSH, but not free radical scavengers, can reverse anticancer effects of PEITC.

5015- Xan,  PEITC,    Comparison of the Impact of Xanthohumol and Phenethyl Isothiocyanate and Their Combination on Nrf2 and NF-κB Pathways in HepG2 Cells In Vitro and Tumor Burden In Vivo
- in-vitro, HCC, HepG2
NRF2↓, Since Nrf2 is overexpressed in HCC its reduced activation together with diminished level of NF-κB by X + PEITC may be considered as a strategy to support conventional HCC therapy.
ROS↑, The increased expression of NQO1 (~90%) was associated with increased ROS generation
NF-kB↓, X + PEITC downregulated NF-κB activation reducing binding of its active subunits to DNA resulting in diminished COX-2 expression.
COX2↓,
Apoptosis↑, In contrast to single phytochemicals, X + PEITC induced apoptosis.
NRF2↑, All phytochemicals enhanced the activation and expression of Nrf2 and its target genes SOD and NQO1 in HepG2 cells
SOD↑,
NQO1↑,


* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 56

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   CYP1A1↑, 1,   CYP2E1↑, 1,   Ferroptosis↑, 2,   GPx↓, 1,   GPx4↓, 1,   GSH↓, 14,   GSH/GSSG↓, 1,   GSSG↓, 1,   GSTA1↓, 1,   GSTP1/GSTπ↑, 1,   H2O2↑, 1,   Iron↑, 1,   lipid-P↑, 2,   MDA↑, 1,   NQO1↑, 2,   Nrf1↑, 1,   NRF2↓, 1,   NRF2↑, 2,   p‑NRF2↑, 1,   OXPHOS↓, 1,   ROS↓, 1,   ROS↑, 24,   mt-ROS↑, 1,   SOD↑, 2,  

Metal & Cofactor Biology ⓘ

TfR1/CD71↑, 1,  

Mitochondria & Bioenergetics ⓘ

AIF↑, 4,   ATP↓, 2,   CDC25↓, 2,   EGF↓, 1,   ETC↓, 1,   mitResp↓, 1,   MKK7↓, 1,   MMP↓, 8,   mtDam↑, 3,   OCR↓, 1,   XIAP↓, 2,  

Core Metabolism/Glycolysis ⓘ

cAMP↓, 1,   cMyc↓, 2,   CYP3A4↓, 1,   Glycolysis↓, 1,  

Cell Death ⓘ

Akt↓, 7,   Apoptosis↓, 1,   Apoptosis↑, 22,   BAX↑, 7,   Bcl-2↓, 5,   Bcl-xL↓, 2,   BID↑, 3,   cl‑BID↑, 1,   BMP2↓, 1,   Casp↑, 1,   Casp3↑, 7,   Casp8↑, 3,   Casp9↑, 5,   Chk2↑, 1,   Cyt‑c↑, 8,   Cyt‑c↝, 1,   Diablo↑, 1,   DR4↑, 4,   DR5↑, 3,   Fas↑, 1,   Ferroptosis↑, 2,   iNOS↓, 1,   JNK↓, 1,   JNK↑, 2,   MAPK↓, 1,   MAPK↑, 1,   Mcl-1↓, 3,   p27↑, 1,   p38↑, 1,   survivin↓, 2,   Telomerase↓, 1,   TumCD↓, 1,   TumCD↑, 4,  

Kinase & Signal Transduction ⓘ

HER2/EBBR2↓, 1,   Sp1/3/4↓, 1,  

Transcription & Epigenetics ⓘ

EZH2↓, 1,   other↝, 2,   TLE1↓, 1,   tumCV↓, 9,  

Protein Folding & ER Stress ⓘ

ATF6↑, 1,   CHOP↑, 1,   ER Stress↑, 1,   GRP78/BiP↑, 2,   PERK↑, 1,   UPR↑, 1,  

Autophagy & Lysosomes ⓘ

TumAuto↑, 4,  

DNA Damage & Repair ⓘ

ATM↑, 1,   DNAdam↑, 3,   P53↓, 1,   P53↑, 8,   cl‑PARP↑, 4,   cl‑PARP1↑, 1,  

Cell Cycle & Senescence ⓘ

CDK1↓, 1,   CDK2↓, 1,   cycD1/CCND1↓, 2,   cycE/CCNE↓, 1,   P21↑, 5,   TumCCA↑, 18,  

Proliferation, Differentiation & Cell State ⓘ

ALDH↓, 4,   BMI1↓, 1,   CD133↓, 1,   CD24↓, 2,   CD34↓, 1,   CD44↓, 3,   CSCs↓, 10,   CSCsMark↓, 2,   EMT↓, 2,   ERK↓, 3,   HDAC↓, 2,   miR-194↑, 1,   mTOR↓, 1,   Nanog↓, 1,   OCT4↓, 1,   PI3K↓, 1,   RAS↓, 1,   SAL↑, 1,   SOX2↓, 1,   STAT3↓, 3,   SUZ12↓, 1,   TumCG↓, 17,  

Migration ⓘ

AP-1↓, 1,   Ca+2↑, 3,   CD11b↓, 1,   E-cadherin↑, 1,   FAK↓, 1,   FTO↓, 1,   ITGB1↓, 1,   ITGB6↓, 1,   Ki-67↓, 2,   MMP2↓, 3,   MMP9↓, 3,   MMPs↓, 1,   N-cadherin↓, 1,   PKCδ↓, 2,   PKCδ↑, 1,   Rho↓, 1,   Slug↓, 1,   Smad1↓, 1,   Smad1↑, 1,   Snail↓, 1,   TGF-β1↓, 1,   TumCI↓, 4,   TumCMig↓, 6,   TumCP↓, 14,   TumMeta↓, 5,   uPA↓, 1,   Vim↓, 1,   Zeb1↓, 1,   ZEB2↓, 1,   α-tubulin↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 4,   EGFR↓, 1,   Hif1a↓, 5,   NO↑, 2,   VEGF↓, 4,  

Barriers & Transport ⓘ

P-gp↓, 1,  

Immune & Inflammatory Signaling ⓘ

CD4+↓, 1,   COX2↓, 3,   IKKα↓, 1,   Inflam↓, 2,   JAK↓, 1,   p‑JAK2↓, 1,   NF-kB↓, 8,   p65↓, 1,  

Hormonal & Nuclear Receptors ⓘ

AR↓, 1,   CDK6↓, 1,   ERα/ESR1↓, 1,  

Drug Metabolism & Resistance ⓘ

ABC↓, 1,   BioAv↑, 2,   BioAv↝, 1,   ChemoSen↑, 8,   CYP1A2↑, 1,   CYP2A3/CYP2A6↓, 1,   Dose↓, 1,   Dose⇅, 1,   Dose↝, 5,   eff↓, 11,   eff↑, 6,   Half-Life↓, 1,   P450↓, 1,   selectivity↑, 11,  

Clinical Biomarkers ⓘ

ALC∅, 1,   AR↓, 1,   EGFR↓, 1,   ERα/ESR1↓, 1,   EZH2↓, 1,   HER2/EBBR2↓, 1,   Ki-67↓, 2,   SUZ12↓, 1,  

Functional Outcomes ⓘ

AntiCan↓, 1,   AntiCan↑, 6,   chemoP↑, 1,   chemoPv↑, 5,   OS↑, 4,   QoL↑, 1,   Risk↓, 5,   toxicity↓, 1,   TumW↓, 1,   Weight↑, 1,  
Total Targets: 200

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   CYP2E1↓, 1,   GPx1↑, 1,   lipid-P↓, 1,   NRF2↑, 1,   ROS↓, 1,   SOD1↑, 1,   SOD2↑, 1,  

Transcription & Epigenetics ⓘ

other↝, 1,  

Proliferation, Differentiation & Cell State ⓘ

Diff↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 2,   BioAv↑, 6,   Dose↝, 3,   Half-Life↝, 1,   P450↓, 1,  

Functional Outcomes ⓘ

chemoPv↑, 2,   Risk↑, 1,   toxicity↓, 1,   toxicity↝, 2,   Weight↓, 1,  
Total Targets: 20

Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include : 
  -low or high Dose
  -format for product, such as nano of lipid formations
  -different cell line effects
  -synergies with other products 
  -if effect was for normal or cancerous cells

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