Curcumin Cancer Research Results

CUR, Curcumin: Click to Expand ⟱
Features:
Curcumin is the main active ingredient in Turmeric. Member of the ginger family.Curcumin is a polyphenol extracted from turmeric with anti-inflammatory and antioxidant properties.
- Has iron-chelating, iron-chelating properties. Ferritin. But still known to increase Iron in Cancer cells.
- GSH depletion in cancer cells, exhaustion of the antioxidant defense system. But still raises GSH↑ in normal cells.
- Higher concentrations (5-10 μM) of curcumin induce autophagy and ROS production
- Inhibition of TrxR, shifting the enzyme from an antioxidant to a prooxidant
- Strong inhibitor of Glo-I, , causes depletion of cellular ATP and GSH
- Curcumin has been found to act as an activator of Nrf2, (maybe bad in cancer cells?), hence could be combined with Nrf2 knockdown
-may suppress CSC: suppresses self-renewal and pathways (Wnt/Notch/Hedgehog).

Curcumin — Curcumin is a turmeric-derived polyphenolic curcuminoid and diarylheptanoid from Curcuma longa, functionally best classified as a natural-product small molecule / nutraceutical candidate with pleiotropic redox, inflammatory, transcriptional, metabolic, and chemosensitizing activity. The standard abbreviation is CUR. It is the principal active pigment of turmeric rhizome, usually studied as purified curcumin, curcuminoid mixtures, turmeric extract, phytosomal curcumin, liposomal curcumin, nanoparticle curcumin, or piperine-enhanced formulations. Its oncology relevance is mechanistically broad but clinically constrained by poor aqueous solubility, rapid metabolism, low free systemic exposure, formulation variability, and insufficient well-powered cancer outcome trials.

Primary mechanisms (ranked):

  1. Suppression of NF-κB / STAT3 inflammatory-survival signaling, reducing cytokine, COX-2, iNOS, anti-apoptotic, invasion, and treatment-resistance programs.
  2. Biphasic redox modulation: ROS buffering in normal/inflamed tissue but ROS↑, GSH depletion, thioredoxin reductase disruption, and oxidative stress amplification in susceptible cancer models at sufficient exposure.
  3. Mitochondrial injury and intrinsic apoptosis, including mitochondrial membrane potential loss, cytochrome-c release, caspase activation, PARP cleavage, and ER-stress/UPR involvement.
  4. PI3K/AKT/mTOR and MAPK pathway modulation, contributing to growth arrest, autophagy modulation, apoptosis sensitization, and reduced survival signaling.
  5. Wnt/β-catenin, Hedgehog/GLI, Notch, and cancer-stem-cell suppression, reducing stemness, EMT, invasion, and recurrence-associated phenotypes in models.
  6. Hypoxia / HIF-1α and glycolysis inhibition, including reduced GLUT1, HK2, LDHA, PKM2, lactate/ECAR, and Warburg-like metabolic support in selected models.
  7. Anti-angiogenic and anti-metastatic modulation, including VEGF, MMPs, uPA, CXCR4/SDF-1, TGF-β/α-SMA, FAK, and EMT-related axes.
  8. Epigenetic and transcriptional reprogramming, including reported HDAC, DNMT, EZH2, Sp-family, p53, and microRNA-related effects.
  9. NRF2 modulation: generally cytoprotective in normal cells but potentially protective for cancer cells when NRF2 is activated; NRF2 suppression/knockdown can increase curcumin-induced ROS stress in some tumor models.
  10. Chemosensitization and radiosensitization, with parallel normal-tissue protective signals reported in some mucositis, dermatitis, oxidative-stress, and radioprotection contexts.

Bioavailability / PK relevance: Conventional oral curcumin has poor systemic bioavailability because of low solubility, low absorption, rapid conjugation, and rapid elimination. Oral trials have used doses up to gram-level daily dosing, but circulating free curcumin is typically low; measured plasma exposure often reflects conjugated curcumin. Piperine, phospholipid/phytosome, micellar, liposomal, nanoparticle, and other enhanced formulations can raise exposure, but each formulation should be treated as a distinct translational entity. Delivery constraints are central for oncology interpretation.

In-vitro vs systemic exposure relevance: Common in-vitro anticancer concentrations, often in the low-to-mid micromolar range and sometimes higher, frequently exceed achievable free plasma exposure from standard oral curcumin. Therefore, direct systemic anticancer claims from cell culture should be weighted cautiously unless supported by tissue-local exposure, enhanced formulation data, local delivery, IV/liposomal delivery, or clinically measured pharmacodynamic biomarkers.

Clinical evidence status: Preclinical evidence is extensive; human oncology evidence is mainly small human, biomarker, pilot, chemoprevention, adjunctive, symptom-management, and formulation trials. Current authoritative oncology summaries judge evidence inadequate to recommend curcumin-containing products as cancer treatment or as routine adjunct anticancer therapy, although symptom-support areas such as oral mucositis, radiation dermatitis, oxidative-status measures, and quality of life have more suggestive but still confirmatory-level evidence.


Clinical studies testing curcumin in cancer patients have used a range of dosages, often between 500 mg and 8 g per day; however, many studies note that doses on the lower end may not achieve sufficient plasma concentrations for a therapeutic anticancer effect in humans.
• Formulations designed to improve curcumin absorption (like curcumin combined with piperine, nanoparticle formulations, or liposomal curcumin) are often employed in clinical trials to enhance its bioavailability.

-Note half-life 6 hrs.
BioAv is poor, use piperine or other enhancers
Pathways:
- induce ROS production at high concentration. Lowers ROS at lower concentrations
curcumin can act as a pro-oxidant when blue light is applied
- ROS↑ related: MMP↓(ΔΨm), ER Stress↑, UPR↑, GRP78↑, Cyt‑c↑, Caspases↑, DNA damage↑, cl-PARP↑, HSP↓
- Lowers AntiOxidant defense in Cancer Cells: GSH↓ Catalase↓ HO1↓ GPx↓
but conversely is known as a NRF2↑ activator in cancer
- Raises AntiOxidant defense in Normal Cells: ROS↓, NRF2↑, SOD↑, GSH↑, Catalase↑,
- lowers Inflammation : NF-kB↓, COX2↓, p38↓, Pro-Inflammatory Cytokines : TNF-α↓, IL-6↓, IL-8↓
- inhibit Growth/Metastases : TumMeta↓, TumCG↓, EMT↓, MMPs↓, MMP2↓, MMP9↓, uPA↓, VEGF↓, NF-κB↓, CXCR4↓, SDF1↓, TGF-β↓, α-SMA↓, ERK↓
- reactivate genes thereby inhibiting cancer cell growth : HDAC↓, DNMT1↓, DNMT3A↓, EZH2↓, P53↑, HSP↓, Sp proteins↓,
- cause Cell cycle arrest : TumCCA↑, cyclin D1↓, CDK2↓, CDK4↓, CDK6↓,
- inhibits Migration/Invasion : TumCMig↓, TumCI↓, ERK↓, EMT↓, TOP1↓, TET1↓,
- inhibits glycolysis /Warburg Effect and ATP depletion : HIF-1α↓, PKM2↓, cMyc↓, GLUT1↓, LDHA↓, HK2↓, PFKs↓, PDKs↓, HK2↓, ECAR↓, OXPHOS↓, GRP78↑, GlucoseCon↓
- inhibits angiogenesis↓ : VEGF↓, HIF-1α↓, Notch↓, FGF↓, PDGF↓, EGFR↓, Integrins↓,
- inhibits Cancer Stem Cells : CSC↓, CK2↓, Hh↓, GLi1↓, CD133↓, CD24↓, β-catenin↓, n-myc↓, sox2↓, OCT4↓,
- Others: PI3K↓, AKT↓, JAK↓, STAT↓, Wnt↓, β-catenin↓, AMPK↓, ERK↓, JNK, TrxR**,
- Synergies: chemo-sensitization, chemoProtective, RadioSensitizer, RadioProtective, Others(review target notes), Neuroprotective, Cognitive, Renoprotection, Hepatoprotective, CardioProtective,

- Selectivity: Cancer Cells vs Normal Cells

Curcumin Cancer Mechanism Ranking

Rank Pathway / Axis Cancer Cells Normal Cells TSF Primary Effect Notes / Interpretation
1 NF-κB / STAT3 inflammatory survival signaling NF-κB ↓; STAT3 ↓; IL-6/TNF-α/COX-2/iNOS ↓; Bcl-2/Bcl-xL/survivin programs ↓ Inflammatory tone ↓; tissue-protective anti-inflammatory effect likely context-dependent R/G Reduced survival, inflammation, invasion, and therapy-resistance signaling Most central and industry-relevant axis; explains many downstream effects but is not curcumin-specific.
2 Biphasic redox stress and antioxidant buffering ROS ↑ (dose-dependent); GSH ↓; antioxidant reserve ↓; oxidative apoptosis ↑ ROS ↓; NRF2/SOD/GSH/catalase/HO-1 often ↑ in stress models R/G Selective redox pressure in susceptible tumor cells with normal-cell protection in lower-stress settings Direction depends strongly on concentration, formulation, light exposure, basal redox state, and tumor antioxidant capacity.
3 Thioredoxin reductase and GSH linked redox systems TrxR inhibition or redox cycling ↑; GSH depletion ↑; oxidative stress ↑ Usually buffered or antioxidant response ↑ at non-toxic exposure R/G Collapse of tumor redox compensation Mechanistically important for ROS amplification and radiosensitization; achievable exposure remains a major constraint.
4 Mitochondrial depolarization and intrinsic apoptosis ΔΨm ↓; cytochrome-c ↑; caspase-3/9 ↑; PARP cleavage ↑; apoptosis ↑ Generally ↔ or protected under oxidative/inflammatory stress R/G Execution of apoptosis after upstream redox and survival-signal disruption Central cytotoxic endpoint in many cell models; often downstream of ROS, ER stress, AKT/mTOR suppression, or p53 modulation.
5 PI3K / AKT / mTOR and autophagy balance PI3K ↓; AKT ↓; mTOR ↓; survival signaling ↓; autophagy ↑ or mixed Stress-adaptive autophagy ↔ or ↑ (context-dependent) R/G Growth suppression and apoptosis sensitization Autophagy may be cytotoxic or protective depending on model and timing; combination logic may require autophagy-state interpretation.
6 Wnt / β-catenin / Hedgehog / Notch stemness signaling β-catenin ↓; GLI/Hedgehog ↓; Notch ↓; CD133/CD44/OCT4/SOX2-like stemness markers ↓ Generally ↔; possible normal stem-cell effects are tissue/context-dependent G Reduced cancer stemness, EMT, self-renewal, and recurrence-associated phenotypes Important for anti-metastatic and anti-CSC positioning; evidence is mainly preclinical.
7 HIF-1α / glycolysis / Warburg metabolism HIF-1α ↓; GLUT1 ↓; HK2 ↓; LDHA ↓; PKM2 ↓; lactate/ECAR ↓; ATP stress ↑ Metabolic effects ↔ or adaptive; normal-cell toxicity depends on exposure G Reduced hypoxic adaptation and glycolytic energy support Mechanistically relevant but formulation and tissue exposure are critical; hypoxic tumors may be more relevant than normoxic cell culture.
8 EMT / invasion / metastasis matrix axis EMT ↓; MMP2/MMP9 ↓; uPA ↓; FAK ↓; CXCR4/SDF-1 ↓; migration/invasion ↓ Inflammation-linked remodeling ↓; wound-healing effects context-dependent G Anti-invasive and anti-metastatic phenotype Strongly supported in models; clinical anti-metastatic efficacy is not established.
9 VEGF / angiogenesis / hypoxia interface VEGF ↓; HIF-1α ↓; angiogenic signaling ↓ Angiogenesis modulation ↔ or ↓ (context-dependent) G Reduced tumor vascular-support signaling Overlaps with NF-κB, HIF-1α, STAT3, and inflammatory cytokine suppression.
10 Epigenetic and transcriptional reprogramming HDAC ↓; DNMT1/3A ↓; EZH2 ↓; Sp proteins ↓; p53 ↑ or restored in selected models Broad transcriptional effects possible; selectivity uncertain G Reactivation of growth-control and differentiation-associated programs Biologically plausible but highly model-dependent; direct target specificity is lower than pathway-level interpretation.
11 Ferroptosis and iron redox stress Iron/redox stress ↑; lipid peroxidation ↑; GPX4/GSH axis may ↓ (model-dependent) Iron-chelation and antioxidant protection may occur (context-dependent) R/G Potential ferroptosis contribution in susceptible tumor models Curcumin can behave as an iron chelator, antioxidant, or pro-oxidant depending on exposure, formulation, and cancer redox context.
12 NRF2 cytoprotection risk NRF2 ↑ may protect tumor cells; NRF2 depletion can enhance curcumin-induced ROS stress in some models NRF2 ↑ supports antioxidant and anti-inflammatory tissue protection G Dual-edged stress-response modulation Important caution for antioxidant matrix use: NRF2 activation is favorable in normal-cell protection but may be undesirable in NRF2-addicted tumors.
13 Chemosensitization and radiosensitization Chemo response ↑; radiation response ↑; apoptosis ↑; resistance pathways ↓ Chemo/radiation injury may ↓ in mucositis, dermatitis, and oxidative-stress contexts R/G Adjunct sensitization with possible normal-tissue protection Attractive translational axis, but clinical evidence remains mainly pilot/small-study; interaction risk should be checked per regimen.
14 Clinical Translation Constraint Free systemic exposure often insufficient for direct cytotoxic extrapolation from in-vitro micromolar data Enhanced formulations may improve exposure but may also alter safety, liver-risk profile, and interaction potential G Bioavailability and formulation dominate translational interpretation Separate ordinary curcumin, turmeric extract, piperine-enhanced, phytosomal, micellar, liposomal, nanoparticle, and IV/liposomal products where possible.

TSF legend:

P: 0–30 min

R: 30 min–3 hr

G: >3 hr
Scientific Papers found: Click to Expand⟱
146- CUR,  EGCG,    Synergistic effect of curcumin on epigallocatechin gallate-induced anticancer action in PC3 prostate cancer cells
- in-vitro, Pca, PC3 - in-vitro, Pca, LNCaP - in-vitro, Pca, DU145
P21↑, TumCCA↑, TumCP↓, BioAv↓,
122- CUR,  isoFl,    Combined inhibitory effects of soy isoflavones and curcumin on the production of prostate-specific antigen
- Human, Pca, LNCaP
PSA↓, AR↓,
123- CUR,    Synthesis of novel 4-Boc-piperidone chalcones and evaluation of their cytotoxic activity against highly-metastatic cancer cells
- in-vitro, Colon, LoVo - in-vitro, Colon, COLO205 - in-vitro, Pca, PC3 - in-vitro, Pca, 22Rv1
NF-kB↓, ATF3↑, HO-1↑, Wnt↓, Akt↓, mTOR↓, PTEN↑, Apoptosis↑, TGF-β↓, PPARγ↑,
124- CUR,    Curcumin-Gene Expression Response in Hormone Dependent and Independent Metastatic Prostate Cancer Cells
- in-vitro, Pca, LNCaP - in-vitro, Pca, C4-2B
TGF-β↓, Wnt↓, PI3k/Akt/mTOR↓, NF-kB↓, PTEN↑, Apoptosis↑, TumCCA↑,
125- CUR,    Bioactivity of Curcumin on the Cytochrome P450 Enzymes of the Steroidogenic Pathway
- in-vitro, adrenal, H295R
CYP17A1↓, CYP19↓, *Nrf1↑, *NF-kB↓, angioG↓, Apoptosis↑, AR↓, toxicity↓, BioAv↑,
126- CUR,    Modulation of miR-34a in curcumin-induced antiproliferation of prostate cancer cells
- in-vitro, Pca, 22Rv1 - in-vitro, Pca, PC3 - in-vitro, Pca, DU145
miR-34a↑, β-catenin/ZEB1↓, cMyc↓, P21↑, cycD1/CCND1↓, PCNA↓, TumCG↓,
127- CUR,    The chromatin remodeling protein BRG1 links ELOVL3 trans-activation to prostate cancer metastasis
- in-vitro, Pca, DU145
Elvol3↓, p300↓,
128- CUR,  RES,    Evaluation of biophysical as well as biochemical potential of curcumin and resveratrol during prostate cancer
- in-vivo, Pca, NA
lipid-P↓, chemoPv↑, GSH↑, SOD↑, GSTs↑, glucose↓,
129- CUR,    Curcumin suppressed the prostate cancer by inhibiting JNK pathways via epigenetic regulation
- vitro+vivo, Pca, LNCaP
JNK↓, H3K4↓, TumCG↓, Apoptosis↑, eff↑,
414- CUR,    Transcriptome Investigation and In Vitro Verification of Curcumin-Induced HO-1 as a Feature of Ferroptosis in Breast Cancer Cells
- in-vitro, BC, MCF-7 - in-vitro, BC, MDA-MB-231
Ferroptosis↑, Iron↑, ROS↑, lipid-P↑, MDA↑, GSH↓, HO-1↑, NRF2↑, GPx↓, ROS↑, Iron↑, GPx4↓, HSP70/HSPA5↑, ATFs↑, CHOP↑, MDA↑, FTL↑, FTH1↑, BACH1↑, REL↑, USF1↑, NFE2L2↑,
182- CUR,  RES,  GI,    Chemopreventive anti-inflammatory activities of curcumin and other phytochemicals mediated by MAP kinase phosphatase-5 in prostate cells
- in-vitro, Pca, DU145 - in-vitro, Pca, PC3 - in-vitro, Pca, LNCaP - in-vitro, Pca, LAPC-4
p38↓, MKP5↑, TNF-α↓, COX2↓, NF-kB↓,
158- CUR,    Curcumin-targeting pericellular serine protease matriptase role in suppression of prostate cancer cell invasion, tumor growth, and metastasis
- vitro+vivo, Pca, LNCaP - in-vitro, Pca, PC3
MMP9↓, Matr↓, Inflam↓, antiOx↓, NF-kB↓, COX2↓, iNOS↓, TumCMig↓, TumCI↓,
404- CUR,    Curcumin induces ferroptosis in non-small-cell lung cancer via activating autophagy
- vitro+vivo, Lung, A549 - vitro+vivo, Lung, H1299
TumAuto↑, TumCG↓, TumCP↓, Iron↑, GSH↓, lipid-P↑, GPx↓, mtDam↑, autolysosome↑, Beclin-1↑, LC3s↑, p62↓, Ferroptosis↑,
405- CUR,  5-FU,    Curcumin activates a ROS/KEAP1/NRF2/miR-34a/b/c cascade to suppress colorectal cancer metastasis
- vitro+vivo, CRC, HCT116
Apoptosis↑, TumCMig↓, NRF2↑, ROS↑, MET↑, miR-34a↑,
406- CUR,    Effect of curcumin on normal and tumor cells: Role of glutathione and bcl-2
- in-vitro, BC, MCF-7 - in-vitro, Hepat, HepG2
GSH↓, Apoptosis↑, Bcl-2↓, cMyc↓,
407- CUR,    Curcumin inhibited growth of human melanoma A375 cells via inciting oxidative stress
- in-vitro, Melanoma, A375
Apoptosis↑, ROS↑, GSH↓, MMP↓,
408- CUR,    Cytotoxic, chemosensitizing and radiosensitizing effects of curcumin based on thioredoxin system inhibition in breast cancer cells: 2D vs. 3D cell culture system
- in-vitro, BC, MCF-7
Trx1↓,
409- CUR,    Curcumin Inhibits Glyoxalase 1—A Possible Link to Its Anti-Inflammatory and Anti-Tumor Activity
- in-vitro, Pca, PC3 - in-vitro, BC, MDA-MB-231
GLO-I↓, GSH↓, ATP↓,
410- CUR,    Nrf2 depletion enhanced curcumin therapy effect in gastric cancer by inducing the excessive accumulation of ROS
- vitro+vivo, GC, AGS - vitro+vivo, GC, HGC27
ROS↑, NRF2↑, eff↓, eff↑,
411- CUR,    Curcumin inhibits the invasion and metastasis of triple negative breast cancer via Hedgehog/Gli1 signaling pathway
- in-vitro, BC, MDA-MB-231
HH↓, EMT↓, Gli1↓,
412- CUR,    Curcumin and Its New Derivatives: Correlation between Cytotoxicity against Breast Cancer Cell Lines, Degradation of PTP1B Phosphatase and ROS Generation
- in-vitro, BC, MCF-7 - in-vitro, BC, MDA-MB-231
ROS↑, PTP1B↓,
413- CUR,    Curcumin attenuates lncRNA H19-induced epithelial-mesenchymal transition in tamoxifen-resistant breast cancer cells
- in-vitro, BC, MCF-7
N-cadherin↓, E-cadherin↑, H19↓,
183- CUR,    Curcumin down-regulates AR gene expression and activation in prostate cancer cell lines
- in-vitro, Pca, LNCaP - in-vitro, Pca, PC3
AR↓, AP-1↓, NF-kB↓, CBP↓,
415- CUR,    Curcumin inhibits proteasome activity in triple-negative breast cancer cells through regulating p300/miR-142-3p/PSMB5 axis
- vitro+vivo, BC, MDA-MB-231
PSMB5↓, CT-I↓, miR-142-3p↑, EP300↓,
417- CUR,    Curcumin inhibits the growth of triple‐negative breast cancer cells by silencing EZH2 and restoring DLC1 expression
- vitro+vivo, BC, MCF-7 - vitro+vivo, BC, MDA-MB-231 - vitro+vivo, BC, MDA-MB-468
EZH2↓, DLC1↑, cycA1/CCNA1↓, CDK1↓, Bcl-2↓, Casp9↑, DLC1↑,
420- CUR,    Anti-metastasis activity of curcumin against breast cancer via the inhibition of stem cell-like properties and EMT
- in-vitro, BC, MCF-7 - in-vitro, BC, MDA-MB-231
Vim↓, Fibronectin↓, β-catenin/ZEB1↓, E-cadherin↓, CD44↑, CD24↓, OCT4↓, Nanog↓, SOX2↓,
422- CUR,    Curcumin induces re-expression of BRCA1 and suppression of γ synuclein by modulating DNA promoter methylation in breast cancer cell lines
- in-vitro, BC, HCC-38 - in-vitro, BC, T47D
BRCA1↑, TET1↑, DNMT3A↑, DNMT1↓, SNCG↓, miR-29b↓, miR-29b↑,
423- CUR,    Inhibition of TLR4/TRIF/IRF3 Signaling Pathway by Curcumin in Breast Cancer Cells
- in-vitro, BC, MCF-7 - in-vitro, BC, MDA-MB-231
TLR4↓, IRF3↓, IFN-γ↓, TRIF↓,
424- CUR,    Curcumin inhibits autocrine growth hormone-mediated invasion and metastasis by targeting NF-κB signaling and polyamine metabolism in breast cancer cells
- in-vitro, BC, MCF-7 - in-vitro, BC, MDA-MB-231
Src↓, p‑STAT1↓, p‑Akt↓, p‑p44↓, p‑p42↓, RAS↓, Raf↓, Vim↓, β-catenin/ZEB1↓, P53↓, Bcl-2↓, Mcl-1↓, PIAS-3↑, SOCS-3↑, SOCS1↑, ROS↑, NF-kB↓, PAO↑, SSAT↑, P21↑, Bak↑,
425- CUR,    Curcumin inhibits proliferation and promotes apoptosis of breast cancer cells
- in-vitro, BC, T47D - in-vitro, BC, MCF-7 - in-vitro, BC, MDA-MB-231 - in-vitro, BC, MDA-MB-468
CDC25↓, cDC2↓, P21↑, p‑Akt↓, p‑mTOR↓, Bcl-2↓, BAX↑, Casp3↑,
426- CUR,    Use of cancer chemopreventive phytochemicals as antineoplastic agents
- in-vitro, BC, MDA-MB-231 - in-vitro, BC, CAL51
Bcl-2↓, ROS↑, BAX↑, RAD51↑, γH2AX↑,
427- CUR,    Curcumin suppresses the malignancy of non-small cell lung cancer by modulating the circ-PRKCA/miR-384/ITGB1 pathway
- in-vitro, Lung, H1299 - in-vitro, Lung, H460 - vitro+vivo, Lung, A549
ITGB1↓, circ-PRKCA↓, miR-384↑,
429- CUR,    TAp63α Is Involved in Tobacco Smoke-Induced Lung Cancer EMT and the Anti-cancer Activity of Curcumin via miR-19 Transcriptional Suppression
- in-vitro, Lung, H1299 - in-vitro, Lung, A549
TAp63α↑, E-cadherin↑, ZO-1↑, Vim↓, N-cadherin↓, miR-19b↓,
430- CUR,    Curcumin suppresses tumor growth of gemcitabine-resistant non-small cell lung cancer by regulating lncRNA-MEG3 and PTEN signaling
- vitro+vivo, Lung, A549
PTEN↑, MEG3↑,
431- CUR,    Curcumin suppresses the stemness of non-small cell lung cancer cells via promoting the nuclear-cytoplasm translocation of TAZ
- in-vitro, Lung, A549 - in-vitro, Lung, H1299
ALDH1A1↓, CD133↓, EpCAM↓, OCT4↓, TAZ↓, Hippo↑, p‑TAZ↑,
167- CUR,    Curcumin-induced apoptosis in PC3 prostate carcinoma cells is caspase-independent and involves cellular ceramide accumulation and damage to mitochondria
- in-vitro, Pca, PC3
MAPK↑, JNK↑, Casp3↑, Casp8↑, Casp9↑, AIF↑, GSH↓, eff↓, Apoptosis↑, DNAdam↑,
159- CUR,    Crosstalk from survival to necrotic death coexists in DU-145 cells by curcumin treatment
- in-vitro, Pca, DU145
ROS↑, p‑Jun↑, p‑p38↑, TumAuto↑, Casp8↑, Casp9↑, Akt↓, ERK↓, p38↓,
160- CUR,    Curcumin inhibits prostate cancer metastasis in vivo by targeting the inflammatory cytokines CXCL1 and -2
- in-vitro, Pca, NA
CXCc↓, IκB↓, NF-kB↓, COX2↓, SPARC↓, EFEMP↓, IKKα↓,
161- CUR,  MeSA,    Enhanced apoptotic effects by the combination of curcumin and methylseleninic acid: potential role of Mcl-1 and FAK
- in-vitro, BC, MDA-MB-231 - in-vitro, Pca, DU145
Mcl-1↑, Mcl-1↓, MPT↑, AIF↑, chemoPv↑, Apoptosis↑, ROS↑, FAK↓, STAT3↓, NF-kB↓,
162- CUR,  EGCG,  SFN,    Shattering the underpinnings of neoplastic architecture in LNCap: synergistic potential of nutraceuticals in dampening PDGFR/EGFR signaling and cellular proliferation
- in-vitro, Pca, LNCaP
p‑PDGF↓,
163- CUR,    Epigenetic CpG Demethylation of the Promoter and Reactivation of the Expression of Neurog1 by Curcumin in Prostate LNCaP Cells
- in-vitro, Pca, LNCaP
MeCP2↓, Neurog1↑, HDAC↓,
164- CUR,    Anti-tumor activity of curcumin against androgen-independent prostate cancer cells via inhibition of NF-κB and AP-1 pathway in vitro
- in-vitro, Pca, PC3
NF-kB↓, AP-1↓, TumCG↓, TumCCA↑,
165- CUR,    Curcumin interrupts the interaction between the androgen receptor and Wnt/β-catenin signaling pathway in LNCaP prostate cancer cells
- in-vitro, Pca, LNCaP
AR↓, β-catenin/ZEB1↓, p‑Akt↓, GSK‐3β↓, p‑β-catenin/ZEB1↑, cycD1/CCND1↓, cMyc↓, chemoPv↑, TumCP↓,
181- CUR,    The effects of curcumin on the invasiveness of prostate cancer in vitro and in vivo
- vitro+vivo, Pca, DU145
MMP2↓, MMP9↓, TumCP↓, TumCI↓,
168- CUR,    Curcumin inhibits Akt/mammalian target of rapamycin signaling through protein phosphatase-dependent mechanism
- in-vitro, Pca, PC3
Akt↓, mTOR↓, AMPK↑, TAp63α↑, TumCP↓,
169- CUR,    Curcumin inhibits the expression of vascular endothelial growth factor and androgen-independent prostate cancer cell line PC-3 in vitro
- in-vitro, Pca, PC3
VEGF↓,
170- CUR,    Curcumin sensitizes TRAIL-resistant xenografts: molecular mechanisms of apoptosis, metastasis and angiogenesis
- vitro+vivo, Pca, PC3
TRAILR↑, BAX↑, P21↑, p27↑, NF-kB↓, cycD1/CCND1↓, VEGF↓, uPA↓, MMP2↓, MMP9↓, Bcl-2↓, Bcl-xL↓,
1617- EA,  CUR,    The inhibition of human glutathione S-transferases activity by plant polyphenolic compounds ellagic acid and curcumin
- in-vitro, Nor, NA
Dose∅, GSTs↓,
1619- EA,  CUR,    Antimutagenic Effect of the Ellagic Acid and Curcumin Combinations
- in-vitro, Nor, NA
eff↑,
649- EGCG,  CUR,  PI,    Targeting Cancer Hallmarks with Epigallocatechin Gallate (EGCG): Mechanistic Basis and Therapeutic Targets
- Review, Var, NA
*BioEnh↑, EGFR↓, HER2/EBBR2↓, IGF-1↓, MAPK↓, ERK↓, RAS↓, Raf↓, NF-kB↓, p‑pRB↓, TumCCA↑, Glycolysis↓, Warburg↓, HK2↓, Pyruv↓,

Showing Research Papers: 251 to 300 of 329
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* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 329

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

antiOx↓, 1,   ATF3↑, 1,   Ferroptosis↑, 2,   GPx↓, 2,   GPx4↓, 1,   GSH↓, 6,   GSH↑, 1,   GSTs↓, 1,   GSTs↑, 1,   HO-1↑, 2,   Iron↑, 3,   lipid-P↓, 1,   lipid-P↑, 2,   MDA↑, 2,   NFE2L2↑, 1,   NRF2↑, 3,   PAO↑, 1,   ROS↑, 10,   SOD↑, 1,   Trx1↓, 1,  

Metal & Cofactor Biology ⓘ

FTH1↑, 1,   FTL↑, 1,  

Mitochondria & Bioenergetics ⓘ

AIF↑, 2,   ATP↓, 1,   CDC25↓, 1,   MKP5↑, 1,   MMP↓, 1,   MPT↑, 1,   mtDam↑, 1,   p‑p42↓, 1,   Raf↓, 2,  

Core Metabolism/Glycolysis ⓘ

AMPK↑, 1,   cMyc↓, 3,   Elvol3↓, 1,   GLO-I↓, 1,   glucose↓, 1,   Glycolysis↓, 1,   HK2↓, 1,   PI3k/Akt/mTOR↓, 1,   PPARγ↑, 1,   PSMB5↓, 1,   Pyruv↓, 1,   SSAT↑, 1,   Warburg↓, 1,  

Cell Death ⓘ

Akt↓, 3,   p‑Akt↓, 3,   Apoptosis↑, 9,   Bak↑, 1,   BAX↑, 3,   Bcl-2↓, 6,   Bcl-xL↓, 1,   Casp3↑, 2,   Casp8↑, 2,   Casp9↑, 3,   CBP↓, 1,   Ferroptosis↑, 2,   Hippo↑, 1,   iNOS↓, 1,   JNK↓, 1,   JNK↑, 1,   MAPK↓, 1,   MAPK↑, 1,   Mcl-1↓, 2,   Mcl-1↑, 1,   MEG3↑, 1,   p27↑, 1,   p38↓, 2,   p‑p38↑, 1,   TRAILR↑, 1,  

Kinase & Signal Transduction ⓘ

HER2/EBBR2↓, 1,  

Transcription & Epigenetics ⓘ

EZH2↓, 1,   H19↓, 1,   H3K4↓, 1,   Matr↓, 1,   MeCP2↓, 1,   p‑pRB↓, 1,   USF1↑, 1,  

Protein Folding & ER Stress ⓘ

ATFs↑, 1,   CHOP↑, 1,   HSP70/HSPA5↑, 1,  

Autophagy & Lysosomes ⓘ

autolysosome↑, 1,   Beclin-1↑, 1,   LC3s↑, 1,   p62↓, 1,   TumAuto↑, 2,  

DNA Damage & Repair ⓘ

BRCA1↑, 1,   DNAdam↑, 1,   DNMT1↓, 1,   DNMT3A↑, 1,   P53↓, 1,   PCNA↓, 1,   RAD51↑, 1,   γH2AX↑, 1,  

Cell Cycle & Senescence ⓘ

CDK1↓, 1,   cycA1/CCNA1↓, 1,   cycD1/CCND1↓, 3,   P21↑, 5,   TAp63α↑, 2,   TumCCA↑, 4,  

Proliferation, Differentiation & Cell State ⓘ

ALDH1A1↓, 1,   CD133↓, 1,   CD24↓, 1,   CD44↑, 1,   cDC2↓, 1,   EMT↓, 1,   EP300↓, 1,   EpCAM↓, 1,   ERK↓, 2,   Gli1↓, 1,   GSK‐3β↓, 1,   HDAC↓, 1,   HH↓, 1,   IGF-1↓, 1,   p‑Jun↑, 1,   miR-142-3p↑, 1,   miR-34a↑, 2,   mTOR↓, 2,   p‑mTOR↓, 1,   Nanog↓, 1,   Neurog1↑, 1,   OCT4↓, 2,   p300↓, 1,   PIAS-3↑, 1,   PTEN↑, 3,   RAS↓, 2,   SOX2↓, 1,   Src↓, 1,   p‑STAT1↓, 1,   STAT3↓, 1,   TAZ↓, 1,   p‑TAZ↑, 1,   TumCG↓, 4,   Wnt↓, 2,  

Migration ⓘ

AP-1↓, 2,   BACH1↑, 1,   circ-PRKCA↓, 1,   DLC1↑, 2,   E-cadherin↓, 1,   E-cadherin↑, 2,   EFEMP↓, 1,   FAK↓, 1,   Fibronectin↓, 1,   ITGB1↓, 1,   MET↑, 1,   miR-19b↓, 1,   miR-29b↓, 1,   miR-29b↑, 1,   miR-384↑, 1,   MMP2↓, 2,   MMP9↓, 3,   N-cadherin↓, 2,   p‑p44↓, 1,   p‑PDGF↓, 1,   PTP1B↓, 1,   SPARC↓, 1,   TET1↑, 1,   TGF-β↓, 2,   TumCI↓, 2,   TumCMig↓, 2,   TumCP↓, 5,   uPA↓, 1,   Vim↓, 3,   ZO-1↑, 1,   β-catenin/ZEB1↓, 4,   p‑β-catenin/ZEB1↑, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   EGFR↓, 1,   REL↑, 1,   VEGF↓, 2,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 3,   CXCc↓, 1,   IFN-γ↓, 1,   IKKα↓, 1,   Inflam↓, 1,   IκB↓, 1,   NF-kB↓, 11,   PSA↓, 1,   SOCS-3↑, 1,   SOCS1↑, 1,   TLR4↓, 1,   TNF-α↓, 1,   TRIF↓, 1,  

Protein Aggregation ⓘ

SNCG↓, 1,  

Hormonal & Nuclear Receptors ⓘ

AR↓, 4,   CYP19↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   BioAv↑, 1,   CT-I↓, 1,   CYP17A1↓, 1,   Dose∅, 1,   eff↓, 2,   eff↑, 3,  

Clinical Biomarkers ⓘ

AR↓, 4,   BRCA1↑, 1,   EGFR↓, 1,   EZH2↓, 1,   HER2/EBBR2↓, 1,   PSA↓, 1,  

Functional Outcomes ⓘ

chemoPv↑, 3,   toxicity↓, 1,  

Infection & Microbiome ⓘ

IRF3↓, 1,  
Total Targets: 201

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

Nrf1↑, 1,  

Immune & Inflammatory Signaling ⓘ

NF-kB↓, 1,  

Drug Metabolism & Resistance ⓘ

BioEnh↑, 1,  
Total Targets: 3

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#:65  Target#:%  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

 

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