Apigenin (mainly Parsley) / Cyt‑c Cancer Research Results

Api, Apigenin (mainly Parsley): Click to Expand ⟱
Features:

Apigenin — a plant-derived flavone (4′,5,7-trihydroxyflavone) abundant in parsley/celery/chamomile and other dietary sources, often abbreviated APG (or “Api” in some indexes). It is a small-molecule polyphenol classified as a dietary phytochemical/nutraceutical candidate with broad pleiotropic signaling effects in oncology models (cell-cycle control, apoptosis, inflammatory signaling, metabolic stress, and invasion/angiogenesis programs), but with important translation constraints driven by low aqueous solubility and extensive phase-II conjugation.

Primary mechanisms (ranked):

  1. Pleiotropic pro-apoptotic / cell-cycle checkpoint engagement (mitochondrial apoptosis, caspases; CDK/cyclin suppression; p53 context-dependent)
  2. PI3K–AKT–MAPK signaling suppression with downstream anti-proliferative and anti-migration effects
  3. Inflammation axis suppression (NF-κB; COX-2 and pro-inflammatory cytokine programs)
  4. Redox stress reprogramming (often ROS↑ in cancer models; antioxidant/NRF2 effects are context-dependent and can diverge between cancer vs normal cells)
  5. HIF-1α–glycolysis downshift with ATP stress (model-dependent)
  6. Anti-invasive / anti-EMT programs (FAK/integrins; MMP/uPA; EMT markers)
  7. Epigenetic modulation (HDAC/DNMT/EZH2 axes; context-dependent)
  8. Anti-angiogenic signaling (VEGF/related programs; model-dependent)
  9. Stemness pathway pressure (Hh/GLI, CK2; model-dependent)
  10. Chemo-/death-ligand sensitization (e.g., TRAIL sensitization reported in preclinical systems)

Bioavailability / PK relevance: Oral apigenin exposure is commonly limited by poor water solubility and extensive first-pass metabolism (glucuronidation/sulfation). Human data indicate circulating apigenin is largely present as conjugated metabolites, and dietary intake can yield only low (typically sub-µM) systemic levels; lipidic/self-emulsifying formulations can increase exposure in vivo (formulation-dependent). Reported half-life/kinetic parameters vary widely across studies and matrices.

In-vitro vs systemic exposure relevance: Many anti-cancer in vitro studies use ~10–50+ µM apigenin, which can exceed typical achievable free aglycone systemic levels after oral intake; some effects may therefore be high-concentration or formulation-enabled rather than diet-achievable. Tissue-local exposure (GI lumen, local mucosa) may be higher than plasma, and conjugate biology may contribute (context-dependent).

Clinical evidence status: Predominantly preclinical oncology evidence (cell and animal models) with limited, non-definitive human cancer interventional data; at least one pilot clinical study concept exists/has been registered (status-dependent). Strongest human evidence base is for non-cancer indications and general bioactivity rather than oncology efficacy.

Apigenin present in parsley, celery, chamomile, oranges and beverages such as tea, beer and wine.
"It exhibits cell growth arrest and apoptosis in different types of tumors such as breast, lung, liver, skin, blood, colon, prostate, pancreatic, cervical, oral, and stomach, by modulating several signaling pathways."
-Note half-life reports vary 2.5-90hrs?.
-low solubility of apigenin in water : BioAv (improves when mixed with oil/dietary fat or lipid based formulations)
-best oil might be MCT oils (medium-chain fatty acids)


Pathways:
- Often considered an antioxidant, in cancer cells it can paradoxically induce ROS production
(one report that goes against most others, by lowering ROS in cancer cells but still effective)
- ROS↑ related: MMP↓(ΔΨm), ER Stress↑, Ca+2↑, Cyt‑c↑, Caspases↑, DNA damage↑, UPR↑, cl-PARP↑, HSP↓
- Lowers AntiOxidant defense in Cancer Cells: NRF2↓, GSH↓ (Conflicting evidence about Nrf2)
        - Combined with Metformin (reduces Nrf2) amplifies ROS production in cancer cells while sparing normal cells.
- Raises AntiOxidant defense in Normal Cells: NRF2↑, SOD↑, GSH↑, Catalase↑,
- lowers Inflammation : NF-kB↓, COX2↓, p38↓, Pro-Inflammatory Cytokines : IL-1β↓, TNF-α↓, IL-6↓, IL-8↓
- inhibit Growth/Metastases : , MMPs↓, MMP2↓, MMP9↓, IGF-1↓, uPA↓, VEGF↓, ERK↓
- reactivate genes thereby inhibiting cancer cell growth : HDAC↓, DNMT1↓, DNMT3A↓, EZH2↓, P53↑, HSP↓
- cause Cell cycle arrest : TumCCA↑, cyclin D1↓, cyclin E↓, CDK2↓, CDK4↓, CDK6↓,
- inhibits Migration/Invasion : TumCMig↓, TumCI↓, FAK↓, ERK↓,
- inhibits glycolysis and ATP depletion : HIF-1α↓, PKM2↓, cMyc↓, PDK1↓, GLUT1↓, LDHA↓, HK2↓, Glucose↓, GlucoseCon↓
- inhibits angiogenesis↓ : VEGF↓, HIF-1α↓, PDGF↓, EGFR↓, Integrins↓,
- inhibits Cancer Stem Cells : CSC↓, CK2↓, Hh↓, GLi↓, GLi1↓,
- Others: PI3K↓, AKT↓, JAK↓, 1, 2, 3, STAT↓, 1, 2, 3, 4, 5, 6, Wnt↓, β-catenin↓, AMPK↓,, α↓,, ERK↓, 5↓, JNK↓,
- Shown to modulate the nuclear translocation of SREBP-2 (related to cholesterol).
- Synergies: chemo-sensitization, chemoProtective, RadioSensitizer, RadioProtective, Others(review target notes)
        -Ex: other flavonoids(chrysin, Luteolin, querectin) curcumin, metformin, sulforaphane, ASA
Neuroprotective, Renoprotection, Hepatoprotective, CardioProtective,
- Selectivity: Cancer Cells vs Normal Cells

Apigenin exhibits biological effects (anticancer, anti-inflammatory, antioxidant, neuroprotective, etc.) typically at concentrations roughly in the range of 1–50 µM.

Parsley microgreens can contain up to 2-3 times more apigenin than mature parsley.
Apigenin is typically measured in the range of 1-10 μM for biological activity. Assuming a molecular weight of 270 g/mol for apigenin, we can estimate the following μM concentrations:
10uM*5L(blood)*270g/mol=13.5mg apigenin (assumes 100% bioavailability)
then an estimated 10-20 mg of apigenin per 100 g of fresh weight parlsey
2.2mg/g of apigenin fresh parsley
45mg/g of apigenin in dried parsley (wikipedia)
so 100g of parsley might acheive 10uM blood serum level (100% bioavailability)
BUT bioavailability is only 1-5%
(Supplements available in 75mg liposomal)( Apigenin Pro Liposomal, 200 mg from mcsformulas.com)

A study had 2g/kg bw (meaning 160g for 80kg person) delivered a maximum 0.13uM of plasma concentration @ 7.2hrs.
Assuming parsley is 90-95% water, then that would be ~16g of dried parsley
Conclusion: to reach 10uM would seem very difficult by oral ingestion of parsley.
Other quotes:
      “4g of dried parsley will be enough for 50kg adult”
      5mg/kg BW yields 16uM, so 80Kg person means 400mg (if dried parsley is 130mg/g, then would need 3g/d)
In many cancer cell lines, concentrations in the range of approximately 20–40 µM have been reported to shift apigenin’s activity from mild antioxidant effects (or negligible ROS changes) toward a clear pro-oxidant effect with measurable ROS increases.

Low doses: At lower concentrations, apigenin is more likely to exhibit its antioxidant properties, scavenging ROS and protecting cells from oxidative stress.
In normal cells with robust antioxidant systems, apigenin’s antioxidant effects might prevail, whereas cancer cells—often characterized by an already high level of basal ROS—can be pushed over the oxidative threshold by increased ROS production induced by apigenin.
In environments with lower free copper levels, this pro-oxidant activity is less pronounced, and apigenin may tilt the balance toward its antioxidant function.

Apigenin — cancer-relevant mechanistic pathway matrix

Rank Pathway / Axis Cancer Cells Normal Cells TSF Primary Effect Notes / Interpretation
1 Mitochondrial apoptosis program ΔΨm ↓, Cyt-c ↑, Caspase cascade ↑, apoptosis ↑ ↔ to protective (model-dependent) R Pro-apoptotic stress commitment Frequently reported core phenotype across tumor models; may be downstream of ROS and kinase-network suppression.
2 Cell-cycle control Cyclin D1/E ↓, CDK2/4/6 ↓, arrest ↑ ↔ G Anti-proliferative checkpointing Often couples to p53/p21 context and growth-factor signaling downshift.
3 PI3K / AKT / MAPK PI3K ↓, AKT ↓, ERK ↓ (model-dependent) ↔ R Growth and survival signaling suppression High industry relevance; provides a convergent explanation for anti-growth and anti-migration phenotypes.
4 NF-κB / COX-2 inflammatory axis NF-κB ↓, COX-2 ↓, inflammatory cytokine programs ↓ Inflammatory tone ↓ G Anti-inflammatory microenvironment pressure Relevant to tumor-promoting inflammation and stromal signaling (context-dependent).
5 ROS modulation ROS ↑ (often), DNA damage ↑, ER stress ↑ (model-dependent) ROS injury ↓ / antioxidant support ↑ (context-dependent) P Redox stress bifurcation (tumor vs normal) Frequently described “paradox”: pro-oxidant stress in tumors while normal cells may show antioxidant protection; not universal.
6 NRF2 / antioxidant defense NRF2 ↓, GSH ↓ (often) ↔ (conflicting) NRF2 ↑, SOD ↑, GSH ↑ (context-dependent) G Antioxidant program reprogramming Direction is context- and model-dependent; important for interpreting chemo-compatibility and ROS claims.
7 HIF-1α / glycolysis HIF-1α ↓, glycolysis ↓, ATP ↓ (model-dependent) ↔ G Metabolic stress / Warburg pressure Reported suppression of glycolysis nodes (e.g., GLUT1/LDHA/HK2/PKM2/PDK1) in some models; may be concentration-sensitive.
8 Migration / invasion and EMT EMT ↓, FAK ↓, integrin signaling ↓, MMPs ↓, uPA ↓ ↔ G Anti-metastatic phenotypes Often downstream of kinase-network suppression and inflammatory tone changes.
9 Angiogenesis programs VEGF ↓ (model-dependent) ↔ G Anti-angiogenic signaling pressure Usually indirect via HIF-1α / inflammatory signaling and tumor-stromal coupling.
10 Epigenetic regulation HDAC ↓, DNMTs ↓, EZH2 ↓ (model-dependent) ↔ G Transcriptional reprogramming Mechanistically plausible but often secondary to upstream stress/kinase changes; evidence varies by model.
11 Cancer stemness pathways Hh/GLI ↓, CK2 ↓, CSC phenotypes ↓ (model-dependent) ↔ G Stemness pressure Typically preclinical; may matter for recurrence-resistance hypotheses.
12 Chemosensitization / death-ligand sensitization Sensitization ↑ (model-dependent) ↔ R Combination leverage Examples include TRAIL sensitization in vitro; translation depends on achievable exposure and interaction risk.
13 Clinical Translation Constraint Low solubility; conjugation-heavy PK; in-vitro concentration gap; potential CYP/UGT/SULT interactions Drug–supplement interaction risk relevant to both — Delivery and interaction limitations Oral free-aglycone systemic levels are often low; formulation can change exposure. In vitro CYP inhibition is reported (notably CYP3A4/2C9); apigenin can also inhibit conjugation pathways in models—caution with narrow-therapeutic-index drugs.

TSF

P: 0–30 min
R: 30 min–3 hr
G: >3 hr
Cyt‑c, cyt-c Release into Cytosol: Click to Expand ⟱
Source:
Type:
Cytochrome c
** The term "release of cytochrome c" ** an increase in level for the cytosol.
Small hemeprotein found loosely associated with the inner membrane of the mitochondrion where it plays a critical role in cellular respiration. Cytochrome c is highly water-soluble, unlike other cytochromes. It is capable of undergoing oxidation and reduction as its iron atom converts between the ferrous and ferric forms, but does not bind oxygen. It also plays a major role in cell apoptosis.

The term "release of cytochrome c" refers to a critical step in the process of programmed cell death, also known as apoptosis.
In its new location—the cytosol—cytochrome c participates in the apoptotic signaling pathway by helping to form the apoptosome, which activates caspases that execute cell death.
Cytochrome c is a small protein normally located in the mitochondrial intermembrane space. Its primary role in healthy cells is to participate in the electron transport chain, a process that helps produce energy (ATP) through oxidative phosphorylation.
Mitochondrial outer membrane permeability leads to the release of cytochrome c from the mitochondria into the cytosol.
The release of cytochrome c is a pivotal event in apoptosis where cytochrome c moves from the mitochondria to the cytosol, initiating a chain reaction that leads to programmed cell death.

On the one hand, cytochrome c can promote cancer cell survival and proliferation by regulating the activity of various signaling pathways, such as the PI3K/AKT pathway. This can lead to increased cell growth and resistance to apoptosis, which are hallmarks of cancer.
On the other hand, cytochrome c can also induce apoptosis in cancer cells by interacting with other proteins, such as Apaf-1 and caspase-9. This can lead to the activation of the intrinsic apoptotic pathway, which can result in the death of cancer cells.
Overexpressed in Breast, Lung, Colon, and Prostrate.
Underexpressed in Ovarian, and Pancreatic.
Scientific Papers found: Click to Expand⟱
1565- Api,    Apigenin-7-glucoside induces apoptosis and ROS accumulation in lung cancer cells, and inhibits PI3K/Akt/mTOR pathway
- in-vitro, Lung, A549 - in-vitro, Nor, BEAS-2B - in-vitro, Lung, H1975
TumCP↓, Apoptosis↑, TumCMig↓, TumCI↓, Cyt‑c↑, MDA↑, GSH↓, ROS↑, PI3K↓, Akt↓, mTOR↓,
1564- Api,    Apigenin-induced prostate cancer cell death is initiated by reactive oxygen species and p53 activation
- in-vitro, Pca, 22Rv1 - in-vivo, NA, NA
MDM2↓, NF-kB↓, p65↓, P21↑, ROS↑, GSH↓, MMP↓, Cyt‑c↑, Apoptosis↑, P53↑, eff↓, Bcl-xL↓, Bcl-2↓, BAX↑, Casp↑, TumCG↓, TumVol↓, TumW↓,
1563- Api,  MET,    Metformin-induced ROS upregulation as amplified by apigenin causes profound anticancer activity while sparing normal cells
- in-vitro, Nor, HDFa - in-vitro, PC, AsPC-1 - in-vitro, PC, MIA PaCa-2 - in-vitro, Pca, DU145 - in-vitro, Pca, LNCaP - in-vivo, NA, NA
selectivity↑, selectivity↑, selectivity↓, ROS↑, eff↑, tumCV↓, MMP↓, Dose∅, eff↓, DNAdam↑, Apoptosis↑, TumAuto↑, Necroptosis↑, p‑P53↑, BIM↑, BAX↑, p‑PARP↑, Casp3↑, Casp8↑, Casp9↑, Cyt‑c↑, Bcl-2↓, AIF↑, p62↑, LC3B↑, MLKL↑, p‑MLKL↓, RIP3↑, p‑RIP3↑, TumCG↑, TumW↓,
1560- Api,    Apigenin as an anticancer agent
- Review, NA, NA
Apoptosis↑, Casp3∅, Casp8∅, TNF-α∅, Cyt‑c↑, MMP2↓, MMP9↓, Snail↓, Slug↓, NF-kB↓, p50↓, PI3K↓, Akt↓, p‑Akt↓,
1547- Api,    Apigenin: Molecular Mechanisms and Therapeutic Potential against Cancer Spreading
- Review, NA, NA
angioG↓, EMT↓, CSCs↓, TumCCA↑, Dose∅, ROS↑, MMP↓, Catalase↓, GSH↓, PI3K↓, Akt↓, NF-kB↓, OCT4↓, Nanog↓, SIRT3↓, SIRT6↓, eff↑, eff↑, Cyt‑c↑, Bax:Bcl2↑, p‑GSK‐3β↓, FOXO3↑, p‑STAT3↓, MMP2↓, MMP9↓, COX2↓, MMPs↓, NRF2↓, HDAC↓, Telomerase↓, eff↑, eff↑, eff↑, eff↑, eff↑, XIAP↓, survivin↓, CK2↓, HSP90↓, Hif1a↓, FAK↓, EMT↓,
2633- Api,    Apigenin induces ROS-dependent apoptosis and ER stress in human endometriosis cells
- in-vitro, EC, NA
TumCP↓, TumCCA↑, MMP↓, Ca+2↑, BAX↑, Cyt‑c↑, ROS↑, lipid-P↑, ER Stress↑, UPR↑, p‑ERK↓, ERK↓, JNK↑,
2640- Api,    Apigenin: A Promising Molecule for Cancer Prevention
- Review, Var, NA
chemoPv↑, ITGB4↓, TumCI↓, TumMeta↓, Akt↓, ERK↓, p‑JNK↓, *Inflam↓, *PKCδ↓, *MAPK↓, EGFR↓, CK2↓, TumCCA↑, CDK1↓, P53↓, P21↑, Bax:Bcl2↑, Cyt‑c↑, APAF1↑, Casp↑, cl‑PARP↑, VEGF↓, Hif1a↓, IGF-1↓, IGFBP3↑, E-cadherin↑, β-catenin/ZEB1↓, HSPs↓, Telomerase↓, FASN↓, MMPs↓, HER2/EBBR2↓, CK2↓, eff↑, AntiAg↑, eff↑, FAK↓, ROS↑, Bcl-2↓, Cyt‑c↑, cl‑Casp3↑, cl‑Casp7↑, cl‑Casp8↑, cl‑Casp9↑, cl‑IAP2↑, AR↓, PSA↓, p‑pRB↓, p‑GSK‐3β↓, CDK4↓, ChemoSen↑, Ca+2↑, cal2↑,
2639- Api,    Plant flavone apigenin: An emerging anticancer agent
- Review, Var, NA
*antiOx↑, *Inflam↓, AntiCan↑, ChemoSen↑, BioEnh↑, chemoPv↑, IL6↓, STAT3↓, NF-kB↓, IL8↓, eff↝, Akt↓, PI3K↓, HER2/EBBR2↓, cycD1/CCND1↓, CycD3↓, p27↑, FOXO3↑, STAT3↓, MMP2↓, MMP9↓, VEGF↓, Twist↓, MMP↓, ROS↑, NADPH↑, NRF2↓, SOD↓, COX2↓, p38↑, Telomerase↓, HDAC↓, HDAC1↓, HDAC3↓, Hif1a↓, angioG↓, uPA↓, Ca+2↑, Bax:Bcl2↑, Cyt‑c↑, Casp9↑, Casp12↑, Casp3↑, cl‑PARP↑, E-cadherin↑, β-catenin/ZEB1↓, cMyc↓, CDK4↓, CDK2↓, CDK6↓, IGF-1↓, CK2↓, CSCs↓, FAK↓, Gli↓, GLUT1↓,
2634- Api,    Apigenin induces both intrinsic and extrinsic pathways of apoptosis in human colon carcinoma HCT-116 cells
- in-vitro, CRC, HCT116
TumCG↓, TumCCA↑, MMP↓, ROS↑, Ca+2↑, ER Stress↑, mtDam↑, CHOP↑, DR5↑, cl‑BID↑, BAX↑, Cyt‑c↑, cl‑Casp3↑, cl‑Casp8↑, cl‑Casp9↑, Apoptosis↑,
2632- Api,    Apigenin inhibits migration and induces apoptosis of human endometrial carcinoma Ishikawa cells via PI3K-AKT-GSK-3β pathway and endoplasmic reticulum stress
- in-vitro, EC, NA
TumCP↓, TumCCA↑, Apoptosis↑, Bcl-2↓, BAX↑, Bak↑, Casp↑, ER Stress↑, Ca+2↑, ATF4↑, CHOP↑, ROS↑, MMP↓, TumCMig↓, TumCI↓, eff↑, P53↑, P21↑, Cyt‑c↑, Casp9↑, Casp3↑, Bcl-xL↓,
1301- Api,    Bcl-2 inhibitor and apigenin worked synergistically in human malignant neuroblastoma cell lines and increased apoptosis with activation of extrinsic and intrinsic pathways
- in-vitro, neuroblastoma, NA
BAX↑, Bcl-2↓, Cyt‑c↑, cal2↑, Casp3↑,
481- CUR,  CHr,  Api,    Flavonoid-induced glutathione depletion: Potential implications for cancer treatment
- in-vitro, Liver, A549 - in-vitro, Pca, PC3 - in-vitro, AML, HL-60
GSH↓, mtDam↑, MMP↓, Cyt‑c↑,

Showing Research Papers: 1 to 12 of 12

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 12

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

Catalase↓, 1,   GSH↓, 4,   lipid-P↑, 1,   MDA↑, 1,   NRF2↓, 2,   ROS↑, 9,   SIRT3↓, 1,   SOD↓, 1,  

Mitochondria & Bioenergetics ⓘ

AIF↑, 1,   MMP↓, 8,   mtDam↑, 2,   XIAP↓, 1,  

Core Metabolism/Glycolysis ⓘ

cMyc↓, 1,   FASN↓, 1,   NADPH↑, 1,  

Cell Death ⓘ

Akt↓, 5,   p‑Akt↓, 1,   APAF1↑, 1,   Apoptosis↑, 6,   Bak↑, 1,   BAX↑, 6,   Bax:Bcl2↑, 3,   Bcl-2↓, 5,   Bcl-xL↓, 2,   cl‑BID↑, 1,   BIM↑, 1,   Casp↑, 3,   Casp12↑, 1,   Casp3↑, 4,   Casp3∅, 1,   cl‑Casp3↑, 2,   cl‑Casp7↑, 1,   Casp8↑, 1,   Casp8∅, 1,   cl‑Casp8↑, 2,   Casp9↑, 3,   cl‑Casp9↑, 2,   CK2↓, 4,   Cyt‑c↑, 13,   DR5↑, 1,   cl‑IAP2↑, 1,   JNK↑, 1,   p‑JNK↓, 1,   MDM2↓, 1,   MLKL↑, 1,   p‑MLKL↓, 1,   Necroptosis↑, 1,   p27↑, 1,   p38↑, 1,   survivin↓, 1,   Telomerase↓, 3,  

Kinase & Signal Transduction ⓘ

HER2/EBBR2↓, 2,  

Transcription & Epigenetics ⓘ

p‑pRB↓, 1,   tumCV↓, 1,  

Protein Folding & ER Stress ⓘ

CHOP↑, 2,   ER Stress↑, 3,   HSP90↓, 1,   HSPs↓, 1,   UPR↑, 1,  

Autophagy & Lysosomes ⓘ

LC3B↑, 1,   p62↑, 1,   TumAuto↑, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 1,   P53↓, 1,   P53↑, 2,   p‑P53↑, 1,   p‑PARP↑, 1,   cl‑PARP↑, 2,   SIRT6↓, 1,  

Cell Cycle & Senescence ⓘ

CDK1↓, 1,   CDK2↓, 1,   CDK4↓, 2,   cycD1/CCND1↓, 1,   CycD3↓, 1,   P21↑, 3,   TumCCA↑, 5,  

Proliferation, Differentiation & Cell State ⓘ

CSCs↓, 2,   EMT↓, 2,   ERK↓, 2,   p‑ERK↓, 1,   FOXO3↑, 2,   Gli↓, 1,   p‑GSK‐3β↓, 2,   HDAC↓, 2,   HDAC1↓, 1,   HDAC3↓, 1,   IGF-1↓, 2,   IGFBP3↑, 1,   mTOR↓, 1,   Nanog↓, 1,   OCT4↓, 1,   PI3K↓, 4,   STAT3↓, 2,   p‑STAT3↓, 1,   TumCG↓, 2,   TumCG↑, 1,  

Migration ⓘ

AntiAg↑, 1,   Ca+2↑, 5,   cal2↑, 2,   E-cadherin↑, 2,   FAK↓, 3,   ITGB4↓, 1,   MMP2↓, 3,   MMP9↓, 3,   MMPs↓, 2,   RIP3↑, 1,   p‑RIP3↑, 1,   Slug↓, 1,   Snail↓, 1,   TumCI↓, 3,   TumCMig↓, 2,   TumCP↓, 3,   TumMeta↓, 1,   Twist↓, 1,   uPA↓, 1,   β-catenin/ZEB1↓, 2,  

Angiogenesis & Vasculature ⓘ

angioG↓, 2,   ATF4↑, 1,   EGFR↓, 1,   Hif1a↓, 3,   VEGF↓, 2,  

Barriers & Transport ⓘ

GLUT1↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 2,   IL6↓, 1,   IL8↓, 1,   NF-kB↓, 4,   p50↓, 1,   p65↓, 1,   PSA↓, 1,   TNF-α∅, 1,  

Hormonal & Nuclear Receptors ⓘ

AR↓, 1,   CDK6↓, 1,  

Drug Metabolism & Resistance ⓘ

BioEnh↑, 1,   ChemoSen↑, 2,   Dose∅, 2,   eff↓, 2,   eff↑, 11,   eff↝, 1,   selectivity↓, 1,   selectivity↑, 2,  

Clinical Biomarkers ⓘ

AR↓, 1,   EGFR↓, 1,   HER2/EBBR2↓, 2,   IL6↓, 1,   PSA↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 1,   chemoPv↑, 2,   TumVol↓, 1,   TumW↓, 2,  
Total Targets: 149

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,  

Cell Death ⓘ

MAPK↓, 1,  

Migration ⓘ

PKCδ↓, 1,  

Immune & Inflammatory Signaling ⓘ

Inflam↓, 2,  
Total Targets: 4

Scientific Paper Hit Count for: Cyt‑c, cyt-c Release into Cytosol
12 Apigenin (mainly Parsley)
1 Metformin
1 Curcumin
1 Chrysin
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

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:32  Target#:77  State#:%  Dir#:2
  wNotes=0  sortOrder:rid,rpid

 

Home Page