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⟱
483- CUR,  PDT,    Visible light and/or UVA offer a strong amplification of the anti-tumor effect of curcumin
- in-vivo, NA, A431
TumVol↓, TumCP↓, Apoptosis↑,
474- CUR,    Modification of radiosensitivity by Curcumin in human pancreatic cancer cell lines
- in-vitro, PC, PANC1 - in-vitro, PC, MIA PaCa-2
TumCD↑, Apoptosis↑, DNAdam↑, γH2AX↑, TumCCA↑,
475- CUR,    Curcumin induces apoptotic cell death in human pancreatic cancer cells via the miR-340/XIAP signaling pathway
- in-vitro, PC, PANC1
Apoptosis↑, cl‑Casp3↑, miR-340↑, cl‑PARP↑, XIAP↓,
476- CUR,    The effects of curcumin on proliferation, apoptosis, invasion, and NEDD4 expression in pancreatic cancer
- in-vitro, PC, PATU-8988 - in-vitro, PC, PANC1
TumCMig↓, TumCI↓, Apoptosis↑, NEDD9↓, p‑Akt↓, p‑mTOR↓, PTEN↑, p73↑, β-TRCP↑,
477- CUR,    Curcumin induces G2/M arrest and triggers autophagy, ROS generation and cell senescence in cervical cancer cells
- in-vitro, Cerv, SiHa
TumCP↓, TumCCA↑, Apoptosis↑, TumAuto↑, CycB/CCNB1↓, CDC25↓, ROS↑, p62↑, LC3‑Ⅱ/LC3‑Ⅰ↑, cl‑Casp3↑, cl‑PARP↑, P53↑, P21↑,
478- CUR,    Curcumin decreases epithelial‑mesenchymal transition by a Pirin‑dependent mechanism in cervical cancer cells
- in-vitro, Cerv, SiHa
EMT↓, N-cadherin↓, Vim↓, Slug↓, Zeb1↓, PIR↓, Pirin↓, E-cadherin↑,
479- CUR,    Curcumin Has Anti-Proliferative and Pro-Apoptotic Effects on Tongue Cancer in vitro: A Study with Bioinformatics Analysis and in vitro Experiments
- in-vitro, Tong, CAL27
TumCP↓, TumCMig↓, Apoptosis↑, TumCCA↑, Bcl-2↓, BAX↑, cl‑Casp3↑,
480- CUR,    Curcumin exerts its tumor suppressive function via inhibition of NEDD4 oncoprotein in glioma cancer cells
- in-vitro, GBM, SNB19
TumCP↓, TumCMig↓, Apoptosis↑, TumCCA↑, NEDD9↓, NOTCH1↓, p‑Akt↓,
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↑,
482- CUR,  PDT,    The Antitumor Effect of Curcumin in Urothelial Cancer Cells Is Enhanced by Light Exposure In Vitro
- in-vitro, Bladder, RT112 - in-vitro, Bladder, UMUC3
Apoptosis↑, TumCG↓, TumCP↓,
473- CUR,    Curcumin inhibits epithelial-mesenchymal transition in oral cancer cells via c-Met blockade
- in-vitro, Oral, HSC4 - in-vitro, Oral, Ca9-22
Vim↓, p‑cMET↓, p‑ERK↓, pro‑MMP9↓, E-cadherin↑,
484- CUR,  PDT,    Low concentrations of curcumin induce growth arrest and apoptosis in skin keratinocytes only in combination with UVA or visible light
- in-vitro, Melanoma, NA
Cyt‑c↑, Casp9↑, Casp8↑, NF-kB↓, EGFR↓,
485- CUR,  PDT,    Red Light Combined with Blue Light Irradiation Regulates Proliferation and Apoptosis in Skin Keratinocytes in Combination with Low Concentrations of Curcumin
- in-vitro, Melanoma, NA
NF-kB↓, Casp8↑, Casp9↑, p‑Akt↓, p‑ERK↓,
872- CUR,  RES,    New Insights into Curcumin- and Resveratrol-Mediated Anti-Cancer Effects
- in-vitro, BC, TUBO - in-vitro, BC, SALTO
TumCP↓, tumCV↓, p62↓, p62↑, TumAuto↑, TumAuto↓, ROS↑, ROS↓, CHOP↑,
933- CUR,  EP,    Effective electrochemotherapy with curcumin in MDA-MB-231-human, triple negative breast cancer cells: A global proteomics study
- in-vitro, BC, NA
Apoptosis↑, ALDOA↓, ENO2↓, LDHA↓, LDHB↓, PFKP↓, PGK1↓, PGM1↓, PGAM1↓, OXPHOS↑, TCA↑,
990- CUR,    Curcumin inhibits aerobic glycolysis and induces mitochondrial-mediated apoptosis through hexokinase II in human colorectal cancer cells in vitro
- in-vitro, CRC, HCT116 - in-vitro, CRC, HT-29
HK2↓, Glycolysis↓, Apoptosis↑,
1006- CUR,    The effect of Curcuma longa extract and its active component (curcumin) on gene expression profiles of lipid metabolism pathway in liver cancer cell line (HepG2)
- in-vitro, Liver, HepG2
TumCP↓, PGC1A↑, CPT1A↑, ACOX1↑, SCD1↓, SREBF2↓, DGAT1↓,
1034- CUR,  immuno,    Enhanced anti‐tumor effects of the PD‐1 blockade combined with a highly absorptive form of curcumin targeting STAT3
- in-vivo, NA, NA
DCells↑, T-Cell↑,
1108- CUR,    Curcumin: a potent agent to reverse epithelial-to-mesenchymal transition
- Review, NA, NA
EMT↓,
1383- CUR,  BBR,  RES,    Regulation of GSK-3 activity by curcumin, berberine and resveratrol: Potential effects on multiple diseases
- Review, NA, NA
GSK‐3β↝, ROS↑,
142- CUR,    Effect of curcumin on the interaction between androgen receptor and Wnt/β-catenin in LNCaP xenografts
- in-vivo, Pca, LNCaP
AR↓, PSA↓,
131- CUR,    Modulation of AKR1C2 by curcumin decreases testosterone production in prostate cancer
- vitro+vivo, Pca, LNCaP - vitro+vivo, Pca, 22Rv1
AKR1C2↓, CYP11A1↓, HSD3B↓, DHT↓, testos↓, StAR↓, SRD5A1↑, AR↓, tumCV↓, TumCG↓, Apoptosis↑,
132- CUR,    Targeting multiple pro-apoptotic signaling pathways with curcumin in prostate cancer cells
- in-vitro, Pca, PC3
TumCCA↑, ROS↑, TumAuto↑, UPR↑, ER Stress↑, Casp3↑, Casp9↑, Casp12↑, PARP↑, other↝, GRP78/BiP↑, PDI↑, eIF2α↑, other↝,
133- CUR,    Curcumin inhibits prostate cancer by targeting PGK1 in the FOXD3/miR-143 axis
- in-vitro, Pca, DU145 - in-vitro, Pca, PC3
miR-143↑, PDK1↓, FOXD3↑, TumCP↓, TumCMig↓, *Inflam↓, *antiOx↑, *chemoPv↑, RadioS↑, ChemoSen↑,
134- CUR,  RES,  MEL,  SIL,    Thioredoxin 1 modulates apoptosis induced by bioactive compounds in prostate cancer cells
- in-vitro, Pca, LNCaP - in-vitro, Pca, PC3
Apoptosis↑, ROS↑, Trx1↓, TumCG↓, eff↓, TXNIP↑,
135- CUR,    Curcumin induces apoptosis and protective autophagy in castration-resistant prostate cancer cells through iron chelation
- in-vitro, Pca, DU145 - in-vitro, Pca, PC3
TfR1/CD71↑, IRP1↑, IronCh↑, Casp↑, eff↑,
136- CUR,  docx,    Combinatorial effect of curcumin with docetaxel modulates apoptotic and cell survival molecules in prostate cancer
- in-vitro, Pca, DU145 - in-vitro, Pca, PC3
Bcl-2↓, Bcl-xL↓, Mcl-1↓, BAX↑, BID↑, PARP↑, NF-kB↓, CDK1↓, COX2↓, RTK-RAS↓, PI3K/Akt↓, EGFR↓, HER2/EBBR2↓, P53↑, ChemoSen↑,
137- CUR,    Curcumin induces G0/G1 arrest and apoptosis in hormone independent prostate cancer DU-145 cells by down regulating Notch signaling
- in-vitro, Pca, DU145
NOTCH1↓, cycD1/CCND1↓, CDK2↓, P21↑, p27↑, P53↑, Bcl-2↓, Casp3↑, Casp9↑, TumCCA↑, TumCP↓, Apoptosis↑,
140- CUR,    Curcumin inhibits cancer-associated fibroblast-driven prostate cancer invasion through MAOA/mTOR/HIF-1α signaling
- in-vitro, Pca, PC3
CAFs/TAFs↓, EMT↓, ROS↓, CXCR4↓, IL6↓, MAOA↓, mTOR↓, HIF-1↓,
141- CUR,    Effect of curcumin on Bcl-2 and Bax expression in nude mice prostate cancer
- in-vivo, Pca, PC3
BAX↑, Bcl-2↓, TumCG↓, TumVol↓, TumW↓, Apoptosis↑, AR↓, Ca+2↑, MPT↑,
130- CUR,    Maspin Enhances the Anticancer Activity of Curcumin in Hormone-refractory Prostate Cancer Cells
- in-vitro, Pca, DU145 - in-vitro, Pca, PC3
BAD↝, BAX↝, eff↑,
143- CUR,    Nonautophagic cytoplasmic vacuolation death induction in human PC-3M prostate cancer by curcumin through reactive oxygen species -mediated endoplasmic reticulum stress
- in-vitro, Pca, LNCaP - in-vitro, Pca, DU145 - in-vitro, Pca, PC3
ER Stress↑, CHOP↑, GRP78/BiP↑, ROS↑, LC3II↑, eff↓, tumCV↓,
144- CUR,  Bical,    Combination of curcumin and bicalutamide enhanced the growth inhibition of androgen-independent prostate cancer cells through SAPK/JNK and MEK/ERK1/2-mediated targeting NF-κB/p65 and MUC1-C
- in-vitro, Pca, PC3 - in-vitro, PC, DU145 - in-vitro, PC, LNCaP
p‑ERK↑, p‑JNK↓, MUC1↓, p65↓, AR↓, TumCG↓, MEK↑, SAPK↑,
432- CUR,    Curcumin-Induced Global Profiling of Transcriptomes in Small Cell Lung Cancer Cells
- in-vitro, Lung, H446
Bcl-2↓, cycF↓, LOX1↓, VEGF↓, MRGPRF↓, BAX↑, Cyt‑c↑, miR-548ah-5p↑,
151- CUR,    Curcumin analogues with high activity for inhibiting human prostate cancer cell growth and androgen receptor activation
- in-vitro, Pca, 22Rv1 - in-vitro, Pca, LNCaP
AR↓, PSA↓, Dose↑,
152- CUR,    Anti-cancer activity of curcumin loaded nanoparticles in prostate cancer
- in-vivo, Pca, NA
β-catenin/ZEB1↓, AR↓, STAT3↓, p‑Akt↓, Mcl-1↓, Bcl-xL↓, cl‑PARP↑, miR-21↓, miR-205↑, TumCG↓, TumCP↓, TumCI↓, angioG↓, TumMeta↓,
153- CUR,    Curcumin Inhibits Prostate Cancer Bone Metastasis by Up-Regulating Bone Morphogenic Protein-7 in Vivo
- in-vivo, Pca, C4-2B
PSA↓, TGF-β↓, BMPs↑, TumMeta↓,
154- CUR,    Curcumin inhibits expression of inhibitor of DNA binding 1 in PC3 cells and xenografts
- vitro+vivo, Pca, PC3
Id1↓, TumCG↓,
155- CUR,    Osteopontin and MMP9: Associations with VEGF Expression/Secretion and Angiogenesis in PC3 Prostate Cancer Cells
- in-vitro, Pca, PC3
p‑ERK↓, VEGF↓, angioG↓, MMP2↓, MMP9↓, angioS↑,
157- CUR,    Curcumin induces cell cycle arrest and apoptosis of prostate cancer cells by regulating the expression of IkappaBalpha, c-Jun and androgen receptor
- in-vitro, Pca, LNCaP - in-vitro, Pca, PC3
cJun↓, AR↓,
121- CUR,    Screening for Circulating Tumour Cells Allows Early Detection of Cancer and Monitoring of Treatment Effectiveness: An Observational Study
- in-vivo, Pca, NA
CTC↓,
10- CUR,    Curcumin Suppresses Lung Cancer Stem Cells via Inhibiting Wnt/β-catenin and Sonic Hedgehog Pathways
- in-vitro, Lung, A549 - in-vitro, Lung, H1299
HH↓, Wnt/(β-catenin)↓, Shh↓, Smo↓, Gli1↝, GLI2↝, CSCs↓, CD133↓, CSCsMark↓,
11- CUR,    Curcumin inhibits hypoxia-induced epithelial‑mesenchymal transition in pancreatic cancer cells via suppression of the hedgehog signaling pathway
- in-vitro, PC, PANC1
HH↓, Shh↓, Smo↓, Gli1↓, N-cadherin↓, E-cadherin↑, Vim↓, TumCP↓, TumCMig↓, TumCI↓, EMT↓, chemoPv↑,
12- CUR,    Curcumin inhibits the Sonic Hedgehog signaling pathway and triggers apoptosis in medulloblastoma cells
- in-vitro, MB, DAOY
HH↓, Shh↓, Gli1↓, PTCH1↓, cMyc↓, n-MYC↓, cycD1/CCND1↓, Bcl-2↓, NF-kB↓, Akt↓, β-catenin/ZEB1↓, survivin↓, Apoptosis↑, ChemoSen↑, RadioS↑, eff↑,
13- CUR,    Role of curcumin in regulating p53 in breast cancer: an overview of the mechanism of action
- Review, BC, NA
P53↑, DR5↑, JNK↑, NRF2↑, PPARγ↑, HER2/EBBR2↓, IR↓, ER(estro)↓, Fas↑, PDGF↓, TGF-β↓, FGF↓, EGFR↓, JAK↓, PAK↓, MAPK↓, ATPase↓, COX2↓, MMPs↓, IL1↓, IL2↓, IL5↓, IL6↓, IL8↓, IL12↓, IL18↓, NF-kB↓, NOTCH1↓, STAT1↓, STAT4↓, STAT5↓, STAT3↓,
14- CUR,    Curcumin, a Dietary Component, Has Anticancer, Chemosensitization, and Radiosensitization Effects by Down-regulating the MDM2 Oncogene through the PI3K/mTOR/ETS2 Pathway
- vitro+vivo, Pca, PC3
PI3K/mTOR/ETS2↓, MDM2↓, P21↑, Apoptosis↑, TumCP↓, eff↑, RadioS↑,
15- CUR,  UA,    Effects of curcumin and ursolic acid in prostate cancer: A systematic review
- Review, Pca, NA
NF-kB↝, Akt↝, AR↝, Apoptosis↝, Bcl-2↝, Casp3↝, BAX↝, P21↝, ROS↝, Bcl-xL↝, JNK↝, MMP2↝, P53↝, PSA↝, VEGF↝, COX2↝, cycD1/CCND1↝, EGFR↝, IL6↝, β-catenin/ZEB1↝, mTOR↝, NRF2↝, AP-1↝, Cyt‑c↝, PI3K↝, PTEN↝, Cyc↝, TNF-α↝,
117- CUR,    Increased Intracellular Reactive Oxygen Species Mediates the Anti-Cancer Effects of WZ35 via Activating Mitochondrial Apoptosis Pathway in Prostate Cancer Cells
- in-vivo, Pca, RM-1 - in-vivo, Pca, DU145
ROS↑, tumCV↓, Apoptosis↑, TumCCA↑, Ca+2↑, eff↓, ER Stress↑,
118- CUR,    Curcumin analog WZ35 induced cell death via ROS-dependent ER stress and G2/M cell cycle arrest in human prostate cancer cells
- in-vitro, Pca, PC3 - in-vitro, Pca, DU145
ROS↑, Bcl-2↓, PARP↑, cDC2↓, CycB/CCNB1↓, MDM2↓, eff↓, eIF2α↑, ATF4↑, CHOP↑, ER Stress↑, TumCCA↑,
120- CUR,    A randomized, double-blind, placebo-controlled trial to evaluate the role of curcumin in prostate cancer patients with intermittent androgen deprivation
- Human, Pca, NA
PSA↓, Dose↝,

Showing Research Papers: 201 to 250 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 ⓘ

GSH↓, 1,   IRP1↑, 1,   NRF2↑, 1,   NRF2↝, 1,   OXPHOS↑, 1,   ROS↓, 2,   ROS↑, 8,   ROS↝, 1,   Trx1↓, 1,  

Metal & Cofactor Biology ⓘ

IronCh↑, 1,   TfR1/CD71↑, 1,  

Mitochondria & Bioenergetics ⓘ

CDC25↓, 1,   MEK↑, 1,   MMP↓, 1,   MPT↑, 1,   mtDam↑, 1,   XIAP↓, 1,  

Core Metabolism/Glycolysis ⓘ

ACOX1↑, 1,   ALDOA↓, 1,   cMyc↓, 1,   CPT1A↑, 1,   DGAT1↓, 1,   ENO2↓, 1,   Glycolysis↓, 1,   HK2↓, 1,   IR↓, 1,   LDHA↓, 1,   LDHB↓, 1,   PDK1↓, 1,   PFKP↓, 1,   PGAM1↓, 1,   PGC1A↑, 1,   PGK1↓, 1,   PGM1↓, 1,   PI3K/Akt↓, 1,   PI3K/mTOR/ETS2↓, 1,   PPARγ↑, 1,   SCD1↓, 1,   SREBF2↓, 1,   TCA↑, 1,  

Cell Death ⓘ

Akt↓, 1,   Akt↝, 1,   p‑Akt↓, 4,   Apoptosis↑, 17,   Apoptosis↝, 1,   BAD↝, 1,   BAX↑, 4,   BAX↝, 2,   Bcl-2↓, 7,   Bcl-2↝, 1,   Bcl-xL↓, 2,   Bcl-xL↝, 1,   BID↑, 1,   Casp↑, 1,   Casp12↑, 1,   Casp3↑, 2,   Casp3↝, 1,   cl‑Casp3↑, 3,   Casp8↑, 2,   Casp9↑, 4,   Cyt‑c↑, 3,   Cyt‑c↝, 1,   DR5↑, 1,   Fas↑, 1,   JNK↑, 1,   JNK↝, 1,   p‑JNK↓, 1,   MAPK↓, 1,   Mcl-1↓, 2,   MDM2↓, 2,   miR-548ah-5p↑, 1,   p27↑, 1,   survivin↓, 1,   TumCD↑, 1,   β-TRCP↑, 1,  

Kinase & Signal Transduction ⓘ

FOXD3↑, 1,   HER2/EBBR2↓, 2,   PAK↓, 1,   RTK-RAS↓, 1,  

Transcription & Epigenetics ⓘ

cJun↓, 1,   miR-143↑, 1,   miR-205↑, 1,   miR-21↓, 1,   other↝, 2,   tumCV↓, 4,  

Protein Folding & ER Stress ⓘ

CHOP↑, 3,   eIF2α↑, 2,   ER Stress↑, 4,   GRP78/BiP↑, 2,   UPR↑, 1,  

Autophagy & Lysosomes ⓘ

LC3‑Ⅱ/LC3‑Ⅰ↑, 1,   LC3II↑, 1,   p62↓, 1,   p62↑, 2,   TumAuto↓, 1,   TumAuto↑, 3,  

DNA Damage & Repair ⓘ

DNAdam↑, 1,   P53↑, 4,   P53↝, 1,   p73↑, 1,   PARP↑, 3,   cl‑PARP↑, 3,   SAPK↑, 1,   γH2AX↑, 1,  

Cell Cycle & Senescence ⓘ

CDK1↓, 1,   CDK2↓, 1,   Cyc↝, 1,   CycB/CCNB1↓, 2,   cycD1/CCND1↓, 2,   cycD1/CCND1↝, 1,   cycF↓, 1,   P21↑, 3,   P21↝, 1,   TumCCA↑, 8,  

Proliferation, Differentiation & Cell State ⓘ

CD133↓, 1,   cDC2↓, 1,   p‑cMET↓, 1,   CSCs↓, 1,   CSCsMark↓, 1,   EMT↓, 4,   p‑ERK↓, 3,   p‑ERK↑, 1,   FGF↓, 1,   Gli1↓, 2,   Gli1↝, 1,   GSK‐3β↝, 1,   HH↓, 3,   Id1↓, 1,   mTOR↓, 1,   mTOR↝, 1,   p‑mTOR↓, 1,   n-MYC↓, 1,   NOTCH1↓, 3,   PI3K↝, 1,   Pirin↓, 1,   PTCH1↓, 1,   PTEN↑, 1,   PTEN↝, 1,   Shh↓, 3,   Smo↓, 2,   STAT1↓, 1,   STAT3↓, 2,   STAT4↓, 1,   STAT5↓, 1,   TumCG↓, 7,   Wnt/(β-catenin)↓, 1,  

Migration ⓘ

AKR1C2↓, 1,   AP-1↝, 1,   ATPase↓, 1,   Ca+2↑, 2,   CAFs/TAFs↓, 1,   E-cadherin↑, 3,   GLI2↝, 1,   miR-340↑, 1,   MMP2↓, 1,   MMP2↝, 1,   MMP9↓, 1,   pro‑MMP9↓, 1,   MMPs↓, 1,   MRGPRF↓, 1,   MUC1↓, 1,   N-cadherin↓, 2,   NEDD9↓, 2,   PDGF↓, 1,   PIR↓, 1,   Slug↓, 1,   TGF-β↓, 2,   TumCI↓, 3,   TumCMig↓, 5,   TumCP↓, 12,   TumMeta↓, 2,   TXNIP↑, 1,   Vim↓, 3,   Zeb1↓, 1,   β-catenin/ZEB1↓, 2,   β-catenin/ZEB1↝, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 2,   angioS↑, 1,   ATF4↑, 1,   EGFR↓, 3,   EGFR↝, 1,   HIF-1↓, 1,   LOX1↓, 1,   PDI↑, 1,   VEGF↓, 2,   VEGF↝, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 2,   COX2↝, 1,   CXCR4↓, 1,   DCells↑, 1,   IL1↓, 1,   IL12↓, 1,   IL18↓, 1,   IL2↓, 1,   IL5↓, 1,   IL6↓, 2,   IL6↝, 1,   IL8↓, 1,   JAK↓, 1,   NF-kB↓, 5,   NF-kB↝, 1,   p65↓, 1,   PSA↓, 4,   PSA↝, 1,   T-Cell↑, 1,   TNF-α↝, 1,  

Synaptic & Neurotransmission ⓘ

MAOA↓, 1,  

Hormonal & Nuclear Receptors ⓘ

AR↓, 7,   AR↝, 1,   CYP11A1↓, 1,   DHT↓, 1,   ER(estro)↓, 1,   HSD3B↓, 1,   SRD5A1↑, 1,   StAR↓, 1,   testos↓, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 3,   Dose↑, 1,   Dose↝, 1,   eff↓, 4,   eff↑, 4,   RadioS↑, 3,  

Clinical Biomarkers ⓘ

AR↓, 7,   AR↝, 1,   BMPs↑, 1,   CTC↓, 1,   EGFR↓, 3,   EGFR↝, 1,   HER2/EBBR2↓, 2,   IL6↓, 2,   IL6↝, 1,   PSA↓, 4,   PSA↝, 1,  

Functional Outcomes ⓘ

chemoPv↑, 1,   TumVol↓, 2,   TumW↓, 1,  
Total Targets: 236

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,  

Immune & Inflammatory Signaling ⓘ

Inflam↓, 1,  

Functional Outcomes ⓘ

chemoPv↑, 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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