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⟱
466- CUR,    Curcumin circumvent lactate-induced chemoresistance in hepatic cancer cells through modulation of hydroxycarboxylic acid receptor-1
- in-vitro, Liver, HepG2 - in-vitro, Liver, HuT78
GlucoseCon↓, lactateProd↓, pH↑, NO↑, LAR↓, Hif1a↓, LDHA↓, MCT1↓, MDR1↓, STAT3↓, HCAR1↓,
467- CUR,    Curcumin inhibits liver cancer by inhibiting DAMP molecule HSP70 and TLR4 signaling
- in-vitro, Liver, HepG2
TumCP↓, TumCI↓, TumMeta↓, Apoptosis↑, HSP70/HSPA5↓, e-HSP70/HSPA5↓, TLR4↓,
468- CUR,  5-FU,    Gut microbiota enhances the chemosensitivity of hepatocellular carcinoma to 5-fluorouracil in vivo by increasing curcumin bioavailability
- vitro+vivo, Liver, HepG2 - vitro+vivo, Liver, 402 - vitro+vivo, Liver, Bel7
Apoptosis↑, TumCCA↑, PI3k/Akt/mTOR↓, p‑PI3K↓, Bacteria↑, cl‑Casp3↑,
469- CUR,    The inhibitory effect of curcumin via fascin suppression through JAK/STAT3 pathway on metastasis and recurrence of ovary cancer cells
- in-vitro, Ovarian, SKOV3
fascin↓, STAT3↓, JAK↓,
470- CUR,    Regulation of carcinogenesis and modulation through Wnt/β-catenin signaling by curcumin in an ovarian cancer cell line
- in-vitro, Ovarian, SKOV3
Wnt/(β-catenin)↓, EMT↓, DNMT3A↓, cycD1/CCND1↓, cMyc↓, Fibronectin↓, Vim↓, E-cadherin↑, SFRP5↑,
471- CUR,    Curcumin induces apoptotic cell death and protective autophagy by inhibiting AKT/mTOR/p70S6K pathway in human ovarian cancer cells
- in-vitro, Ovarian, SKOV3 - in-vitro, Ovarian, A2780S
Apoptosis↑, TumAuto↑, p62↓, p‑Akt↓, p‑mTOR↓, p‑P70S6K↓, Casp9↑, PARP↑, ATG3↑, Beclin-1↑, LC3‑Ⅱ/LC3‑Ⅰ↑,
433- CUR,    Curcumin Inhibits the Migration and Invasion of Non-Small-Cell Lung Cancer Cells Through Radiation-Induced Suppression of Epithelial-Mesenchymal Transition and Soluble E-Cadherin Expression
- in-vitro, Lung, A549
E-cadherin↓, Vim↓, Slug↓, N-cadherin↓, Snail↓, MMP9↓, EMT↓,
443- CUR,    Reduced Caudal Type Homeobox 2 (CDX2) Promoter Methylation Is Associated with Curcumin’s Suppressive Effects on Epithelial-Mesenchymal Transition in Colorectal Cancer Cells
- in-vitro, CRC, SW480
DNMT1↓, DNMT3A↓, N-cadherin↓, Vim↓, Wnt↓, Snail↓, Twist↓, β-catenin/ZEB1↓, E-cadherin↑, EMT↓, CDX2↓,
437- CUR,    Anti-cancer activity of amorphous curcumin preparation in patient-derived colorectal cancer organoids
- vitro+vivo, CRC, TCO1 - vitro+vivo, CRC, TCO2
cycD1/CCND1↓, cMyc↓, p‑ERK↓, CD44↓, CD133↓, LGR5↓, TumCCA↑, TumVol↓, CSCs↓,
434- CUR,    Curcumin induces apoptosis in lung cancer cells by 14-3-3 protein-mediated activation of Bad
- in-vitro, Lung, A549
14-3-3 proteins↓, p‑BAD↓, p‑Akt↓, Akt↓, cl‑Casp9↑, cl‑PARP↑,
435- CUR,    Antitumor activity of curcumin by modulation of apoptosis and autophagy in human lung cancer A549 cells through inhibiting PI3K/Akt/mTOR pathway
- in-vitro, Lung, A549
Apoptosis↑, TumAuto↑, LC3‑Ⅱ/LC3‑Ⅰ↑, Beclin-1↑, p62↓, PI3K↓, Akt↓, mTOR↓, p‑Akt↓, p‑mTOR↓,
436- CUR,    Integrated microRNA and gene expression profiling reveals the crucial miRNAs in curcumin anti‐lung cancer cell invasion
- in-vitro, Lung, A549
miR-25-5p↓, miR-330-5p↑, MAPK↓, Wnt↓,
9- CUR,    Curcumin Suppresses Malignant Glioma Cells Growth and Induces Apoptosis by Inhibition of SHH/GLI1 Signaling Pathway in Vitro and Vivo
- vitro+vivo, MG, U87MG - vitro+vivo, MG, T98G
HH↓, Shh↓, Gli1↓, cycD1/CCND1↓, Bcl-2↓, FOXM1↓, Bax:Bcl2↑, TumCP↓, TumCMig↓, Apoptosis↑, TumVol↑, TumCCA↑, Casp3↑, OS↑,
438- CUR,    Curcumin Reduces Colorectal Cancer Cell Proliferation and Migration and Slows In Vivo Growth of Liver Metastases in Rats
- vitro+vivo, CRC, CC531
TumCP↓, TumVol↓, Albumin↑, ALP↑, AST↑, ALAT↑, cholinesterase↓,
439- CUR,    Curcumin suppresses LGR5(+) colorectal cancer stem cells by inducing autophagy and via repressing TFAP2A-mediated ECM pathway
- in-vitro, CRC, LGR5
Apoptosis↑, TumAuto↑, GP1BB↓, COL9A3↓, COMP↓, AGRN↓, ITGB4↓, LAMA5↓, COL2A1↓, ITGB6↓, LGR5↓, TFAP2A↓, ECM/TCF↓,
440- CUR,    Curcumin Reverses NNMT-Induced 5-Fluorouracil Resistance via Increasing ROS and Cell Cycle Arrest in Colorectal Cancer Cells
- vitro+vivo, CRC, SW480 - vitro+vivo, CRC, HT-29
NNMT↓, p‑STAT3↓, TumCP↓, TumCCA↑, ROS↑,
441- CUR,    Curcumin Regulates ERCC1 Expression and Enhances Oxaliplatin Sensitivity in Resistant Colorectal Cancer Cells through Its Effects on miR-409-3p
- in-vitro, CRC, HCT116
ERCC1↓, Bcl-2↓, GSTP1/GSTπ↓, MRP↓, P-gp↓, miR-409-3p↑, survivin↓,
442- CUR,  5-FU,    Curcumin may reverse 5-fluorouracil resistance on colonic cancer cells by regulating TET1-NKD-Wnt signal pathway to inhibit the EMT progress
- in-vitro, CRC, HCT116
Apoptosis↑, TumCP↓, TumCCA↑, TET1↑, NKD2↑, Wnt↓, EMT↓, Vim↑, E-cadherin↓, β-catenin/ZEB1↓, TCF↓, AXIN1↓,
454- CUR,    Curcumin-Induced DNA Demethylation in Human Gastric Cancer Cells Is Mediated by the DNA-Damage Response Pathway
- in-vitro, GC, MGC803
TumCMig↓, TumCP↓, ROS↑, mtDam↑, DNAdam↑, Apoptosis↑, ATR↑, P21↑, p‑P53↑, GADD45A↑, p‑γH2AX↑,
444- CUR,  Cisplatin,    LncRNA KCNQ1OT1 is a key factor in the reversal effect of curcumin on cisplatin resistance in the colorectal cancer cells
- vitro+vivo, CRC, HCT8
TumVol↓, Apoptosis↑, Bcl-2↓, Cyt‑c↑, BAX↑, cl‑Casp3↑, cl‑PARP1↑, miR-497↑, KCNQ1OT1↓,
445- CUR,    Curcumin Regulates the Progression of Colorectal Cancer via LncRNA NBR2/AMPK Pathway
- in-vitro, CRC, HCT116 - in-vitro, CRC, HCT8 - in-vitro, CRC, SW480 - in-vitro, CRC, SW-620
p‑AMPK↑, p‑ACC-α↑, NBR2↑, p‑S6K↓, mTOR↓,
446- CUR,    The Influence of Curcumin on the Downregulation of MYC, Insulin and IGF-1 Receptors: A Possible Mechanism Underlying the Anti-Growth and Anti-Migration in Chemoresistant Colorectal Cancer Cells
- in-vitro, CRC, SW480
IR↓, IGF-1↓, Myc↓, TumCMig↓, TumCP↓,
447- CUR,  OXA,    Curcumin reverses oxaliplatin resistance in human colorectal cancer via regulation of TGF-β/Smad2/3 signaling pathway
- vitro+vivo, CRC, HCT116
p‑p65↓, Bcl-2↓, Casp3↑, EMT↓, p‑SMAD2↓, p‑SMAD3↓, N-cadherin↓, TGF-β↓, E-cadherin↑, TumVol↓, TumCMig↓,
448- CUR,    Heat shock protein 27 influences the anti-cancer effect of curcumin in colon cancer cells through ROS production and autophagy activation
- in-vitro, CRC, HT-29
Apoptosis↑, TumCCA↑, p‑Akt↓, Akt↓, Bcl-2↓, p‑BAD↓, BAD↑, cl‑PARP↑, ROS↑, HSP27↑, Beclin-1↑, p62↑, GPx1↓, GPx4↓,
449- CUR,    Curcumin Suppresses the Colon Cancer Proliferation by Inhibiting Wnt/β-Catenin Pathways via miR-130a
- vitro+vivo, CRC, SW480
TumCP↓, β-catenin/ZEB1↓, TCF↓, miR-21↓, NKD2↑, miR-130a↓,
450- CUR,    Curcumin may be a potential adjuvant treatment drug for colon cancer by targeting CD44
- in-vitro, CRC, HCT116 - in-vitro, CRC, HCT8
TumCP↓, TumCMig↓, CD44↓, CSCs↓,
451- CUR,    The effect of Curcumin on multi-level immune checkpoint blockade and T cell dysfunction in head and neck cancer
- vitro+vivo, HNSCC, SCC15 - vitro+vivo, HNSCC, SNU1076 - vitro+vivo, HNSCC, SNU1041
TumCMig↓, TumCG↓, PD-L1↓, PD-L2↓, Galectin-9↓, EMT↓, T-Cell↑, TILs↑, PD-1↓, TIM-3↓, CD4+↓, CD25+↓, FoxP3+↓, E-cadherin↑, CD8+↑, IFN-γ↑,
452- CUR,    Curcumin downregulates the PI3K-AKT-mTOR pathway and inhibits growth and progression in head and neck cancer cells
- vitro+vivo, HNSCC, SCC9 - vitro+vivo, HNSCC, FaDu - vitro+vivo, HNSCC, HaCaT
TumCCA↑, PI3k/Akt/mTOR↓, Casp3↑, EGFR↓, EGF↑, PRKCG↑, p‑Akt↓, p‑mTOR↓, RPS6KA1↓, EIF4E↓, proCasp3↓,
453- CUR,    Cellular uptake and apoptotic properties of gemini curcumin in gastric cancer cells
- in-vitro, GC, AGS
Bcl-2↓, survivin↓, BAX↑, TumCCA↑,
1609- CUR,  EA,    Curcumin and Ellagic acid synergistically induce ROS generation, DNA damage, p53 accumulation and apoptosis in HeLa cervical carcinoma cells
- in-vitro, Cerv, NA
eff↑, Dose∅, ROS↑, DNAdam↑, P53↑, P21↑, BAX↑, Dose∅,
1409- CUR,    Curcumin analog WZ26 induces ROS and cell death via inhibition of STAT3 in cholangiocarcinoma
- in-vivo, CCA, Walker256
TumCG↓, ROS↑, MMP↓, STAT3↓, TumCCA↑, eff↓,
1410- CUR,    Curcumin induces ferroptosis and apoptosis in osteosarcoma cells by regulating Nrf2/GPX4 signaling pathway
- vitro+vivo, OS, MG63
tumCV↓, Apoptosis↑, TumCG↓, NRF2↓, GPx4↓, HO-1↓, xCT↓, ROS↑, MDA↑, GSH↓,
1411- CUR,  Cisplatin,    Curcumin and its derivatives in cancer therapy: Potentiating antitumor activity of cisplatin and reducing side effects
- Review, Var, NA
ChemoSen↑, *ROS↓, *NF-kB↓, TumCCA↑,
1418- CUR,    Potential complementary and/or synergistic effects of curcumin and boswellic acids for management of osteoarthritis
- Review, Arthritis, NA
*COX2↓, *Inflam↓, *5LO↓, *NO↓, *NF-kB↓, *TNF-α↓, *IL1↓, *IL2↑, *IL6↓, *IL8↓, *IL12↓, *MCP1↓, *PGE2↓, *MMP2↓, *MMP3↓, *MMP9↓, *NLRP3↓, *ROS↓,
1485- CUR,  Chemo,  Rad,    Curcumin, the golden spice from Indian saffron, is a chemosensitizer and radiosensitizer for tumors and chemoprotector and radioprotector for normal organs
- Review, Var, NA
ChemoSen↑, NF-kB↓, *STAT3↓, *COX2↓, *Akt↓, *NRF2↑, *HO-1↑, *GPx↑, *NADPH↑, *GSH↑, *ROS↓, *p300↓, radioP↑, chemoP↑, RadioS↑,
1486- CUR,    Curcumin and lung cancer--a review
- Review, Lung, NA
RadioS↑, ChemoSen↑,
1487- CUR,    Relationship and interactions of curcumin with radiation therapy
- Review, Var, NA
RadioS↑, ChemoSen↑, NF-kB↓, radioP↑, BioAv↓, *toxicity↓,
1488- CUR,    Anti-Cancer and Radio-Sensitizing Effects of Curcumin in Nasopharyngeal Carcinoma
RadioS↑, ChemoSen↑,
1505- CUR,    Epigenetic targets of bioactive dietary components for cancer prevention and therapy
- Review, NA, NA
TumCCA↑, Apoptosis↑, DNMTs↓, HDAC↓, HATs↓, TumCP↓, p300↓, HDAC1↓, HDAC3↓, HDAC8↓, NF-kB↓,
1510- CUR,  Chemo,    Combination therapy in combating cancer
- Review, NA, NA
*NRF2↑, *GSH↑, *ROS↓, ChemoSideEff↓, eff↑, OS↓, chemoP↑,
1408- CUR,    Antiproliferative and ROS Regulation Activity of Photoluminescent Curcumin-Derived Nanodots
- in-vitro, Lung, A549
ROS↓, ROS↑,
1616- CUR,  EA,    Kinetics of Inhibition of Monoamine Oxidase Using Curcumin and Ellagic Acid
- in-vitro, Nor, NA
*MAOA↓, *Dose∅, Dose?,
1792- CUR,  LEC,    Chondroprotective effect of curcumin and lecithin complex in human chondrocytes stimulated by IL-1β via an anti-inflammatory mechanism
- in-vitro, Arthritis, RAW264.7 - NA, NA, HCC-38
*Inflam↓, *NF-kB↓, *iNOS↓, *COX2↓, *NO↓, *PGE2↓, *MMPs↑, *TIMP1↑, *BioEnh↑,
1809- CUR,  Oxy,    Long-term stabilisation of myeloma with curcumin
- Case Report, Melanoma, NA
*OS↑, QoL↑, Dose↑, Dose↑, IL6↓, STAT3↓, NF-kB↓, COX2↓,
1977- CUR,    Synthesis and evaluation of curcumin analogues as potential thioredoxin reductase inhibitors
- in-vitro, BC, MCF-7 - in-vitro, Cerv, HeLa - in-vitro, Lung, A549
TrxR↓, Dose↝, eff↑,
1978- CUR,    Curcumin targeting the thioredoxin system elevates oxidative stress in HeLa cells
- in-vitro, Cerv, HeLa
TrxR1↓, ROS↑, DNA-PK↑, eff↑, Trx↓, Trx1↓,
1979- CUR,  Rad,    Dimethoxycurcumin, a metabolically stable analogue of curcumin enhances the radiosensitivity of cancer cells: Possible involvement of ROS and thioredoxin reductase
- in-vitro, Lung, A549
eff↑, ROS↑, GSH/GSSG↓, TrxR↓, selectivity↑,
1980- CUR,  Rad,    Thioredoxin reductase-1 (TxnRd1) mediates curcumin-induced radiosensitization of squamous carcinoma cells
- in-vitro, Cerv, HeLa - in-vitro, Laryn, FaDu
selectivity↑, RadioS↑, TrxR↓, ROS↑, ERK↑, Dose∅, cl‑PARP↑,
1981- CUR,    Mitochondrial targeted curcumin exhibits anticancer effects through disruption of mitochondrial redox and modulation of TrxR2 activity
- in-vitro, Lung, NA
eff↑, ROS↑, mt-GSH↓, Bax:Bcl2↑, Cyt‑c↑, MMP↓, Casp3↑, Trx2↓, TrxR↓, mt-DNAdam↑,
1982- CUR,    Inhibition of thioredoxin reductase by curcumin analogs
- in-vitro, NA, NA
eff↑, TrxR↓,

Showing Research Papers: 151 to 200 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 ⓘ

GPx1↓, 1,   GPx4↓, 2,   GSH↓, 1,   mt-GSH↓, 1,   GSH/GSSG↓, 1,   GSTP1/GSTπ↓, 1,   HO-1↓, 1,   MDA↑, 1,   NRF2↓, 1,   ROS↓, 1,   ROS↑, 11,   Trx↓, 1,   Trx1↓, 1,   Trx2↓, 1,   TrxR↓, 5,   TrxR1↓, 1,   xCT↓, 1,  

Mitochondria & Bioenergetics ⓘ

EGF↑, 1,   MMP↓, 2,   mtDam↑, 1,  

Core Metabolism/Glycolysis ⓘ

p‑ACC-α↑, 1,   ALAT↑, 1,   p‑AMPK↑, 1,   cMyc↓, 2,   ERCC1↓, 1,   GlucoseCon↓, 1,   IR↓, 1,   lactateProd↓, 1,   LAR↓, 1,   LDHA↓, 1,   NNMT↓, 1,   PI3k/Akt/mTOR↓, 2,   p‑S6K↓, 1,  

Cell Death ⓘ

14-3-3 proteins↓, 1,   Akt↓, 3,   p‑Akt↓, 5,   Apoptosis↑, 12,   BAD↑, 1,   p‑BAD↓, 2,   BAX↑, 3,   Bax:Bcl2↑, 2,   Bcl-2↓, 6,   Casp3↑, 4,   cl‑Casp3↑, 2,   proCasp3↓, 1,   Casp9↑, 1,   cl‑Casp9↑, 1,   Cyt‑c↑, 2,   MAPK↓, 1,   MCT1↓, 1,   miR-497↑, 1,   Myc↓, 1,   survivin↓, 2,  

Kinase & Signal Transduction ⓘ

miR-25-5p↓, 1,  

Transcription & Epigenetics ⓘ

COMP↓, 1,   HATs↓, 1,   KCNQ1OT1↓, 1,   miR-21↓, 1,   miR-409-3p↑, 1,   tumCV↓, 1,  

Protein Folding & ER Stress ⓘ

HSP27↑, 1,   HSP70/HSPA5↓, 1,   e-HSP70/HSPA5↓, 1,  

Autophagy & Lysosomes ⓘ

ATG3↑, 1,   Beclin-1↑, 3,   LC3‑Ⅱ/LC3‑Ⅰ↑, 2,   p62↓, 2,   p62↑, 1,   TumAuto↑, 3,  

DNA Damage & Repair ⓘ

ATR↑, 1,   DNA-PK↑, 1,   DNAdam↑, 2,   mt-DNAdam↑, 1,   DNMT1↓, 1,   DNMT3A↓, 2,   DNMTs↓, 1,   GADD45A↑, 1,   NBR2↑, 1,   P53↑, 1,   p‑P53↑, 1,   PARP↑, 1,   cl‑PARP↑, 3,   cl‑PARP1↑, 1,   p‑γH2AX↑, 1,  

Cell Cycle & Senescence ⓘ

cycD1/CCND1↓, 3,   P21↑, 2,   TFAP2A↓, 1,   TumCCA↑, 11,  

Proliferation, Differentiation & Cell State ⓘ

AXIN1↓, 1,   CD133↓, 1,   CD44↓, 2,   CDX2↓, 1,   CSCs↓, 2,   EIF4E↓, 1,   EMT↓, 6,   ERK↑, 1,   p‑ERK↓, 1,   FOXM1↓, 1,   Gli1↓, 1,   HDAC↓, 1,   HDAC1↓, 1,   HDAC3↓, 1,   HDAC8↓, 1,   HH↓, 1,   IGF-1↓, 1,   LGR5↓, 2,   miR-330-5p↑, 1,   mTOR↓, 2,   p‑mTOR↓, 3,   NKD2↑, 2,   p300↓, 1,   p‑P70S6K↓, 1,   PI3K↓, 1,   p‑PI3K↓, 1,   PRKCG↑, 1,   RPS6KA1↓, 1,   SFRP5↑, 1,   Shh↓, 1,   STAT3↓, 4,   p‑STAT3↓, 1,   TCF↓, 2,   TumCG↓, 3,   Wnt↓, 3,   Wnt/(β-catenin)↓, 1,  

Migration ⓘ

AGRN↓, 1,   COL2A1↓, 1,   COL9A3↓, 1,   E-cadherin↓, 2,   E-cadherin↑, 4,   fascin↓, 1,   Fibronectin↓, 1,   Galectin-9↓, 1,   GP1BB↓, 1,   ITGB4↓, 1,   ITGB6↓, 1,   LAMA5↓, 1,   miR-130a↓, 1,   MMP9↓, 1,   N-cadherin↓, 3,   Slug↓, 1,   p‑SMAD2↓, 1,   p‑SMAD3↓, 1,   Snail↓, 2,   TET1↑, 1,   TGF-β↓, 1,   TumCI↓, 1,   TumCMig↓, 6,   TumCP↓, 10,   TumMeta↓, 1,   Twist↓, 1,   Vim↓, 3,   Vim↑, 1,   β-catenin/ZEB1↓, 3,  

Angiogenesis & Vasculature ⓘ

ECM/TCF↓, 1,   EGFR↓, 1,   Hif1a↓, 1,   NO↑, 1,  

Barriers & Transport ⓘ

MRP↓, 1,   P-gp↓, 1,  

Immune & Inflammatory Signaling ⓘ

CD25+↓, 1,   CD4+↓, 1,   COX2↓, 1,   FoxP3+↓, 1,   HCAR1↓, 1,   IFN-γ↑, 1,   IL6↓, 1,   JAK↓, 1,   NF-kB↓, 4,   p‑p65↓, 1,   PD-1↓, 1,   PD-L1↓, 1,   PD-L2↓, 1,   T-Cell↑, 1,   TILs↑, 1,   TLR4↓, 1,  

Cellular Microenvironment ⓘ

pH↑, 1,   TIM-3↓, 1,  

Synaptic & Neurotransmission ⓘ

cholinesterase↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   ChemoSen↑, 5,   Dose?, 1,   Dose↑, 2,   Dose↝, 1,   Dose∅, 3,   eff↓, 1,   eff↑, 7,   MDR1↓, 1,   RadioS↑, 5,   selectivity↑, 2,  

Clinical Biomarkers ⓘ

ALAT↑, 1,   Albumin↑, 1,   ALP↑, 1,   AST↑, 1,   EGFR↓, 1,   FOXM1↓, 1,   IL6↓, 1,   Myc↓, 1,   PD-L1↓, 1,  

Functional Outcomes ⓘ

chemoP↑, 2,   ChemoSideEff↓, 1,   OS↓, 1,   OS↑, 1,   QoL↑, 1,   radioP↑, 2,   TumVol↓, 4,   TumVol↑, 1,  

Infection & Microbiome ⓘ

Bacteria↑, 1,   CD8+↑, 1,  
Total Targets: 208

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

GPx↑, 1,   GSH↑, 2,   HO-1↑, 1,   NRF2↑, 2,   ROS↓, 4,  

Core Metabolism/Glycolysis ⓘ

NADPH↑, 1,  

Cell Death ⓘ

Akt↓, 1,   iNOS↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

p300↓, 1,   STAT3↓, 1,  

Migration ⓘ

5LO↓, 1,   MMP2↓, 1,   MMP3↓, 1,   MMP9↓, 1,   MMPs↑, 1,   TIMP1↑, 1,  

Angiogenesis & Vasculature ⓘ

NO↓, 2,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 3,   IL1↓, 1,   IL12↓, 1,   IL2↑, 1,   IL6↓, 1,   IL8↓, 1,   Inflam↓, 2,   MCP1↓, 1,   NF-kB↓, 3,   PGE2↓, 2,   TNF-α↓, 1,  

Synaptic & Neurotransmission ⓘ

MAOA↓, 1,  

Protein Aggregation ⓘ

NLRP3↓, 1,  

Drug Metabolism & Resistance ⓘ

BioEnh↑, 1,   Dose∅, 1,  

Clinical Biomarkers ⓘ

IL6↓, 1,  

Functional Outcomes ⓘ

OS↑, 1,   toxicity↓, 1,  
Total Targets: 35

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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