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⟱
6229- CUR,    Curcumin inhibits NF-kB and Wnt/β-catenin pathways in cervical cancer cells
- in-vitro, Cerv, NA
TumCI↓, TumCP↓, NF-kB↓, Wnt↓, β-catenin/ZEB1↓,
6228- CUR,    A pharmacokinetic study and critical reappraisal of curcumin formulations enhancing bioavailability
- Study, Nor, NA
*BioAv↓, *other↓,
6227- CUR,    Revisiting Curcumin in Cancer Therapy: Recent Insights into Molecular Mechanisms, Nanoformulations, and Synergistic Combinations
- Review, Var, NA
Wnt↓, β-catenin/ZEB1↓, PI3K↓, Akt↓, mTOR↓, JAK↓, STAT3↓, MAPK↓, NF-kB↓, NOTCH↓, TumCG↓, Apoptosis↑, GSK‐3β↓, cMyc↓, survivin↓, Axin2↑, TumCCA↑, PTEN↑, P53↑, ROS↑, Casp3↑, PARP↑, Ferroptosis↑, angioG↓, TumCI↓, TumMeta↓, BioAv↓, Half-Life↓, ChemoSen↑,
6226- CUR,  Rad,    Analysis of Curcumin as a Radiosensitizer in Cancer Therapy with Serum Survivin Examination: Randomised Control Trial
- Trial, Cerv, NA
survivin↓, RadioS↑, toxicity↓,
6225- CUR,    Natural products for enhancing the sensitivity or decreasing the adverse effects of anticancer drugs through regulating the redox balance
- Review, Var, NA
ox-Trx1↑, TrxR1↓, TrxR↓, ROS↑, GSH/GSSG↓, eff↓, Fenton↑, H2O2↑, *NRF2↑, *Keap1↓, *HO-1↑, *NQO1↑, ChemoSen↑,
6224- CUR,    Thioredoxin reductase: An emerging pharmacologic target for radiosensitization of cancer
- Review, Var, NA
RadioS↑, TrxR↓,
6223- CUR,    Curcumin Rewires the Tumor Metabolic Landscape: Mechanisms and Clinical Prospects
- Review, Var, NA
Ferroptosis↑, GutMicro↑, Akt↓, mTOR↓, NF-kB↓, Wnt↓, β-catenin/ZEB1↓, STAT3↓, TumCP↓, TumCI↓, TumMeta↓, AMPK↑, P53↑, NRF2↑, TumCCA↑, Apoptosis↑, Casp↑, GPx4↓, DNMTs↓, HDAC↓, VEGF↓, Imm↑, NK cell↑, Warburg↓, Hif1a↓, HK2↓, PKM2↓, LDHA↓, GLUT1↓, MCT1↓, AMPK↑, FASN↓, SCD1↓, GLS↓, Apoptosis↑, ETC↓, MMP↓, ROS↑, lipid-P↑, ChemoSen↑, PDK1↓, Beclin-1↓, ATP↓, Glycolysis↓, GlucoseCon↓, lactateProd↑, MMPs↓, GSH↓, G6PD↓, OXPHOS↓, SREBP2↓, COX2↓, AP-1↓, NADH↓, NRF2↑, HO-1↑, Iron↑, MDA↑, *ROS↓, *Inflam↓,
6222- CUR,    Anticancer Molecular Mechanisms of Curcuminoids: An Updated Review of Clinical Trials
- Review, Var, NA
RadioS↑, ChemoSen↑, MMPs↓, TumMeta↓, TumCI↓, Inflam↓, NF-kB↓, BioAv↓, BioAv↑, MAPK↓, PI3K↓, Akt↓, *ROS↓, *MDA↓, *lipid-P↓, *Half-Life↓, mTOR↓,
6221- CUR,    Oxidative Stress and Cancer: Harnessing the Therapeutic Potential of Curcumin and Analogues Against Cancer
- Review, Var, NA
NF-kB↓, Imm↑, *TAC↑, *MDA↓, ROS↑, TumAuto↑, TumCCA↑, Keap1↑, ChemoSen↑, ER Stress↑, eff↓, TrxR↓, STAT3↓, *BioAv↓,
6219- CUR,    Natural Products and Altered Metabolism in Cancer: Therapeutic Targets and Mechanisms of Action
- Review, Var, NA
PI3K↓, Akt↓, NF-kB↓, BioAv↑, GSK‐3β↓, Slug↓, Cyt‑c↑, Casp3↑, Casp9↑,
6218- CUR,    Exploring the Thioredoxin System as a Therapeutic Target in Cancer: Mechanisms and Implications
- Review, Var, NA
NF-kB↓, TrxR↓, ROS↑, TumMeta↓, TumCD↑, RadioS↑, BioAv↝, BioAv↑,
6217- CUR,    Curcumin: a therapeutic strategy in cancers by inhibiting the canonical WNT/β-catenin pathway
- Review, Var, NA
Wnt↓, β-catenin/ZEB1↓, PPARγ↑, Akt↓, *ROS↓, *Inflam↓, Bcl-2↓, GSK‐3β↑, NF-kB↓, COX2↓,
5229- CUR,    Activation of Transcription Factor NF-κB Is Suppressed by Curcumin (Diferuloylmethane)
- in-vitro, Melanoma, NA
NF-kB↓,
6215- CUR,    Curcumin: biochemistry, pharmacology, advanced drug delivery systems, and its epigenetic role in combating cancer
- Review, Var, NA
*antiOx↑, *Inflam↓, *BioAv↓, NF-kB↓, PI3K↓, Akt↓, Wnt↓, β-catenin/ZEB1↓, DNMTs↓, TumCI↓, TumMeta↓, *BioAv↑, *BioAv↑, angioG↓, VEGF↓, MMPs↓, *ROS↓, *SOD↑, *Catalase↑, *GSTs↑, *HO-1↑, *NRF2↑, mTOR↓, GSK‐3β↓, FOXO1↓, *radioP↑, *IL1↓, *IL6↓, *TNF-α↓, HATs↓, HDAC↓, ROS↑, ROS↑, MMP↓, Casp↑, Cyt‑c↑, COX1↓, COX2↓, PGE2↓, *cytoP450↓, ChemoSen↑, cardioP↑, eff↑,
6214- CUR,    Curcumin Nanoparticles-related Non-invasive Tumor Therapy, and Cardiotoxicity Relieve
TumCD↓, TumCI↓, *Inflam↓, *antiOx↓, *AntiTum↓, NF-kB↓, COX2↓, Casp9↓, ROS↑, BioAv↑, RadioS↑, ChemoSen↑, Imm↑, PhotoS↑, sonoS↑, 5LO↓, iNOS↓, IL2↓, TNF-α↓, Casp9↑, Casp3↑, Bcl-2↓, BAX↑, Apoptosis↑, ER Stress↑, cycD1/CCND1↓, CDK2↓, CycB/CCNB1↓, TumCCA↑, MMPs↓, *radioP↑, chemoP↑, hepatoP↑, cardioP↑, eff↑, PhotoS↑, eff↑, ROS↑, GSH↓,
6213- CUR,    Potentiality of Curcumin Against Radio-Chemotherapy Induced Oral Mucositis: A Review
- Review, Var, NA
*antiOx↑, *GSH↑, *SOD↑, *Catalase↑, *lipid-P↓, *NF-kB↓, *NRF2↑, *Wound Healing↑, *eff↑,
6212- CUR,  Rad,    Radiosensitization and Radioprotection by Curcumin in Glioblastoma and Other Cancers
- Review, Var, NA
RadioS↑, *radioP↑, EGFR↓, TGF-β↓, ROS↑, P53↑, PI3K↓, NF-kB↓, COX2↓, EMT↓, Hif1a↓, HSP90↓, mTOR↓, *Catalase↑, *SOD↑, *MDA↑, *Wound Healing↑, *hepatoP↑, *NF-kB↓, *ROS↓,
6211- CUR,    The effect of curcumin on hypoxia in the tumour microenvironment as a regulatory factor in cancer
- Review, Var, NA
HIF-1↓, VEGF↓, angioG↓, RadioS↑, ChemoSen↑, other↝, Apoptosis↑, TumCG↓, TumMeta↓, BioAv↓, COX2↓, CD31↓, IL8↓, TGF-β↓, NF-kB↓, JAK2↓, STAT3↓,
6210- CUR,    Potential Roles and Mechanisms of Curcumin and its Derivatives in the Regulation of Ferroptosis
Ferroptosis↑, *Ferroptosis↓, ROS↑, Fenton↑, *IronCh↑, GPx4↓, MDA↑, GSH↓, *NRF2↑, *HO-1↑,
6209- CUR,    Curcumin as a complementary treatment in oncological therapy: a systematic review
other↝, eff↓, *BioAv↓, ChemoSen↓,
6208- CUR,    Memory and Brain Amyloid and Tau Effects of a Bioavailable Form of Curcumin in Non-Demented Adults: A Double-Blind, Placebo-Controlled 18-Month Trial
- Trial, Nor, NA
*memory↑, *Aβ↓, *tau↓,
6207- CUR,    Enhancing the Bioavailability and Bioactivity of Curcumin for Disease Prevention and Treatment
- Review, Var, NA - Review, AD, NA
*AntiCan↑, *Obesity↓, *Inflam↓, *lipid-P↓, *BioAv↓, *BioAv↑, *BioAv↑, *BioAv↑, *BioAv↑, *BioAv↑, *ROS↓, *mt-SOD↑, *MDA↓, *BBB↓, *Aβ↓, *GSK‐3β↓, *tau↓, *neuroG↑, *memory↑, cardioP↑,
6206- CUR,    Bioavailability of Oral Curcumin in Systematic Reviews: A Methodological Study
- Review, Nor, NA
*BioAv↓, *Half-Life↓, *BioAv↑,
6205- CUR,    Clinical trials on curcumin in relation to its bioavailability and effect on malignant diseases: critical analysis
- Review, Var, NA
BioAv↓, Half-Life↓, COX2↓, ChemoSen↑, cachexia↓, NF-kB↓,
6050- CUR,  SeNPs,    Efficacy of curcumin-selenium nanoemulsion in alleviating oxidative damage induced by aluminum chloride in a rat model of Alzheimer's disease
- in-vivo, AD, NA
*cognitive↑, *AChE↓, *Aβ↓, *P53↓, *tau↓, *NRF2↓, *TNF-α↓, *NO↑, *Catalase↑, *antiOx↑, *Inflam↓,
3862- CUR,  RES,    The metalloproteinase ADAM10: A useful therapeutic target?
- Review, AD, NA
*SIRT1↑, *ADAM10↑,
5397- CUR,  SFN,  RES,  EGCG,  Ash  Targeting Cancer Stem Cells with Phytochemicals: Molecular Mechanisms and Therapeutic Potential
- Review, Var, NA
CSCs↓,
2974- CUR,    Curcumin Suppresses Metastasis via Sp-1, FAK Inhibition, and E-Cadherin Upregulation in Colorectal Cancer
- in-vitro, CRC, HCT116 - in-vitro, CRC, HT29 - in-vitro, CRC, HCT15 - in-vitro, CRC, COLO205 - in-vitro, CRC, SW-620 - in-vivo, NA, NA
TumCMig↓, TumCI↓, TumCG↓, TumMeta↓, Sp1/3/4↓, HDAC4↓, FAK↓, CD24↓, E-cadherin↑, EMT↓, TumCP↓, NF-kB↓, AP-1↝, STAT3↓, P53?, β-catenin/ZEB1↓, NOTCH1↝, Hif1a↝, PPARα↝, Rho↓, MMP2↓, MMP9↓,
2816- CUR,    NEUROPROTECTIVE EFFECTS OF CURCUMIN
- Review, AD, NA - Review, Park, NA
*neuroP↑, *Inflam↓, *antiOx↑, *BioAv↓, *AP-1↓, *NF-kB↓, *HATs↓, *HDAC↑, Dose↑, *ROS↓, *cognitive↑, *Aβ↓,
2817- CUR,    Neuroprotection by curcumin: A review on brain delivery strategies
- Review, Nor, NA
*BioAv↝, neuroP↑,
2818- CUR,    Novel Insight to Neuroprotective Potential of Curcumin: A Mechanistic Review of Possible Involvement of Mitochondrial Biogenesis and PI3/Akt/ GSK3 or PI3/Akt/CREB/BDNF Signaling Pathways
- Review, AD, NA
*neuroP↑, *ROS↓, *Inflam↓, *Apoptosis↓, *cognitive↑, *cardioP↑, other↑, *COX2↓, *IL1β↓, *TNF-α↓, NF-kB↓, *PGE2↓, *iNOS↓, *NO↓, *IL2↓, *IL4↓, *IL6↓, *INF-γ↓, *GSK‐3β↓, *STAT↓, *GSH↑, *MDA↓, *lipid-P↓, *SOD↑, *GPx↑, *Catalase↑, *GSR↓, *LDH↓, *H2O2↓, *Casp3↓, *Casp9↓, *NRF2↑, *AIF↓, *ATP↑,
2819- CUR,  Chemo,    Curcumin as a hepatoprotective agent against chemotherapy-induced liver injury
- Review, Var, NA
*hepatoP↑, *Inflam↓, *antiOx↑, *lipid-P↓, *GSH↑, *SOD↑, *Catalase↑, *GPx↑, *GSTs↑, *ROS↓, *ALAT↓, *AST↓, *MDA↓, *NRF2↑, *COX2↑, *NF-kB↓, *ICAM-1↓, *MCP1↓, *HO-1↑, CXCc↓,
2820- CUR,    Hepatoprotective Effect of Curcumin on Hepatocellular Carcinoma Through Autophagic and Apoptic Pathways
- in-vitro, HCC, HepG2
*hepatoP↑, *ROS↓, tumCV↓,
2821- CUR,    Antioxidant curcumin induces oxidative stress to kill tumor cells (Review)
- Review, Var, NA
*antiOx↑, *NRF2↑, *ROS↓, *Inflam↓, ROS↑, p‑ERK↑, ER Stress↑, mtDam↑, Apoptosis↑, Akt↓, mTOR↓, HO-1↑, Fenton↑, GSH↓, Iron↑, p‑JNK↑, Cyt‑c↑, ATF6↑, CHOP↑,
2822- CUR,    Identification of curcumin derivatives as human glyoxalase I inhibitors: A combination of biological evaluation, molecular docking, 3D-QSAR and molecular dynamics simulation studies
- Analysis, Nor, NA
GLO-I↓,
2823- CUR,    Binding of curcumin with glyoxalase I: Molecular docking, molecular dynamics simulations, and kinetics analysis
- Study, Nor, NA
GLO-I↓,
2815- CUR,    Biochemical and cellular mechanism of protein kinase CK2 inhibition by deceptive curcumin
*CK2↑,
2975- CUR,    Curcumin inhibits proliferation, migration and neointimal formation of vascular smooth muscle via activating miR-22
- in-vivo, Nor, NA
*miR-22↑, *Sp1/3/4↓,
2976- CUR,    Curcumin suppresses the proliferation of oral squamous cell carcinoma through a specificity protein 1/nuclear factor‑κB‑dependent pathway
- in-vitro, Oral, HSC3 - in-vitro, HNSCC, CAL33
tumCV↓, Sp1/3/4↓, p65↓, HSF1↓, NF-kB↓,
2977- CUR,    Curcumin Down-Regulates Toll-Like Receptor-2 Gene Expression and Function in Human Cystic Fibrosis Bronchial Epithelial Cells
- in-vitro, CF, NA
*TLR2↓, *Sp1/3/4↓,
2978- CUR,    N-acetyl cysteine mitigates curcumin-mediated telomerase inhibition through rescuing of Sp1 reduction in A549 cells
- in-vitro, Lung, A549
ROS↑, hTERT/TERT↓, Sp1/3/4↓, eff↓,
2979- CUR,  GB,    Curcumin overcome primary gefitinib resistance in non-small-cell lung cancer cells through inducing autophagy-related cell death
- in-vitro, Lung, H157 - in-vitro, Lung, H1299
EGFR↓, Sp1/3/4↓, ERK↓, MEK↓, Akt↓, S6K↓,
2980- CUR,    Inhibition of NF B and Pancreatic Cancer Cell and Tumor Growth by Curcumin Is Dependent on Specificity Protein Down-regulation
- in-vivo, PC, NA
TumCG↓, p50↓, p65↓, NF-kB↓, Sp1/3/4↓, MMP↓, ROS↑,
3860- CUR,    Curcumin Ameliorates Memory Decline via Inhibiting BACE1 Expression and β-Amyloid Pathology in 5×FAD Transgenic Mice
- in-vivo, AD, NA
*Aβ↓, *BACE↓, *memory↑,
3575- CUR,    The curry spice curcumin reduces oxidative damage and amyloid pathology in an Alzheimer transgenic mouse
- in-vivo, AD, NA
*antiOx↑, *ROS↓, *IL1β↓, *Aβ↓, *Inflam↓, *toxicity↓,
2688- CUR,    Effects of resveratrol, curcumin, berberine and other nutraceuticals on aging, cancer development, cancer stem cells and microRNAs
- Review, Var, NA - Review, AD, NA
*ROS↓, *SOD↑, p16↑, JAK2↓, STAT3↓, CXCL12↓, IL6↓, MMP2↓, MMP9↓, TGF-β↓, α-SMA↓, LAMs↓, DNAdam↑, *memory↑, *cognitive↑, *Inflam↓, *antiOx↑, *NO↑, *MDA↓, *ROS↓, DNMT1↓, ROS↑, Casp3↑, Apoptosis↑, miR-21↓, LC3II↓, ChemoSen↑, NF-kB↓, CSCs↓, Nanog↓, OCT4↓, SOX2↓, eff↑, Sp1/3/4↓, miR-27a-3p↓, ZBTB10↑, SOX9?, ChemoSen↑, VEGF↓, XIAP↓, Bcl-2↓, cycD1/CCND1↓, BioAv↑, Hif1a↓, EMT↓, BioAv↓, PTEN↑, VEGF↓, Akt↑, EZH2↓, NOTCH1↓, TP53↑, NQO1↑, HO-1↑,
2304- CUR,    Curcumin decreases Warburg effect in cancer cells by down-regulating pyruvate kinase M2 via mTOR-HIF1α inhibition
- in-vitro, Lung, H1299 - in-vitro, BC, MCF-7 - in-vitro, Cerv, HeLa - in-vitro, Pca, PC3 - in-vitro, Nor, HEK293
Glycolysis↓, GlucoseCon↓, lactateProd↓, PKM2↓, mTOR↓, Hif1a↓, selectivity↑, Dose↝, tumCV↓,
2305- CUR,    Mitochondrial targeting nano-curcumin for attenuation on PKM2 and FASN
- in-vitro, BC, MCF-7
BioAv↑, PKM2↓, FASN↓, Glycolysis↓,
2307- CUR,    Cell-Type Specific Metabolic Response of Cancer Cells to Curcumin
- in-vitro, Colon, HT29 - in-vitro, Laryn, FaDu
PKM2↓, Warburg↓, mTOR↓, Hif1a↓, Glycolysis↓,
2308- CUR,    Counteracting Action of Curcumin on High Glucose-Induced Chemoresistance in Hepatic Carcinoma Cells
- in-vitro, Liver, HepG2
GlucoseCon↓, lactateProd↓, ECAR↓, NO↓, ROS↑, HK2↓, PFK1↓, GAPDH↓, PKM2↓, LDHA↓, FASN↓, GLUT1↓, MCT1↓, MCT4↓, HCAR1↓, SDH↑, ChemoSen↑, ROS↑, BioAv↑, P53↑, NF-kB↓, pH↑,

Showing Research Papers: 51 to 100 of 329
Prev Page 2 of 7 Next

* 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 ⓘ

Fenton↑, 3,   Ferroptosis↑, 3,   GPx4↓, 2,   GSH↓, 4,   GSH/GSSG↓, 1,   H2O2↑, 1,   HO-1↑, 3,   Iron↑, 2,   Keap1↑, 1,   lipid-P↑, 1,   MDA↑, 2,   NADH↓, 1,   NQO1↑, 1,   NRF2↑, 2,   OXPHOS↓, 1,   ROS↑, 17,   ox-Trx1↑, 1,   TrxR↓, 4,   TrxR1↓, 1,  

Mitochondria & Bioenergetics ⓘ

ATP↓, 1,   ETC↓, 1,   MEK↓, 1,   MMP↓, 3,   mtDam↑, 1,   SDH↑, 1,   XIAP↓, 1,  

Core Metabolism/Glycolysis ⓘ

AMPK↑, 2,   cMyc↓, 1,   ECAR↓, 1,   FASN↓, 3,   G6PD↓, 1,   GAPDH↓, 1,   GLO-I↓, 2,   GLS↓, 1,   GlucoseCon↓, 3,   Glycolysis↓, 4,   HK2↓, 2,   lactateProd↓, 2,   lactateProd↑, 1,   LDHA↓, 2,   MCT4↓, 1,   PDK1↓, 1,   PFK1↓, 1,   PKM2↓, 5,   PPARα↝, 1,   PPARγ↑, 1,   S6K↓, 1,   SCD1↓, 1,   SREBP2↓, 1,   Warburg↓, 2,  

Cell Death ⓘ

Akt↓, 8,   Akt↑, 1,   Apoptosis↑, 7,   BAX↑, 1,   Bcl-2↓, 3,   Casp↑, 2,   Casp3↑, 4,   Casp9↓, 1,   Casp9↑, 2,   Cyt‑c↑, 3,   Ferroptosis↑, 3,   hTERT/TERT↓, 1,   iNOS↓, 1,   p‑JNK↑, 1,   MAPK↓, 2,   MCT1↓, 2,   survivin↓, 2,   TumCD↓, 1,   TumCD↑, 1,  

Kinase & Signal Transduction ⓘ

SOX9?, 1,   Sp1/3/4↓, 6,  

Transcription & Epigenetics ⓘ

EZH2↓, 1,   HATs↓, 1,   miR-21↓, 1,   miR-27a-3p↓, 1,   other↑, 1,   other↝, 2,   PhotoS↑, 2,   sonoS↑, 1,   tumCV↓, 3,  

Protein Folding & ER Stress ⓘ

ATF6↑, 1,   CHOP↑, 1,   ER Stress↑, 3,   HSF1↓, 1,   HSP90↓, 1,  

Autophagy & Lysosomes ⓘ

Beclin-1↓, 1,   LC3II↓, 1,   TumAuto↑, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 1,   DNMT1↓, 1,   DNMTs↓, 2,   p16↑, 1,   P53?, 1,   P53↑, 4,   PARP↑, 1,   TP53↑, 1,  

Cell Cycle & Senescence ⓘ

CDK2↓, 1,   CycB/CCNB1↓, 1,   cycD1/CCND1↓, 2,   TumCCA↑, 4,  

Proliferation, Differentiation & Cell State ⓘ

Axin2↑, 1,   CD24↓, 1,   CSCs↓, 2,   EMT↓, 3,   ERK↓, 1,   p‑ERK↑, 1,   FOXO1↓, 1,   GSK‐3β↓, 3,   GSK‐3β↑, 1,   HDAC↓, 2,   HDAC4↓, 1,   mTOR↓, 8,   Nanog↓, 1,   NOTCH↓, 1,   NOTCH1↓, 1,   NOTCH1↝, 1,   OCT4↓, 1,   PI3K↓, 5,   PTEN↑, 2,   SOX2↓, 1,   STAT3↓, 6,   TumCG↓, 4,   Wnt↓, 5,  

Migration ⓘ

5LO↓, 1,   AP-1↓, 1,   AP-1↝, 1,   CD31↓, 1,   CXCL12↓, 1,   E-cadherin↑, 1,   FAK↓, 1,   LAMs↓, 1,   MMP2↓, 2,   MMP9↓, 2,   MMPs↓, 4,   Rho↓, 1,   Slug↓, 1,   TGF-β↓, 3,   TumCI↓, 7,   TumCMig↓, 1,   TumCP↓, 3,   TumMeta↓, 7,   α-SMA↓, 1,   β-catenin/ZEB1↓, 6,  

Angiogenesis & Vasculature ⓘ

angioG↓, 3,   EGFR↓, 2,   HIF-1↓, 1,   Hif1a↓, 5,   Hif1a↝, 1,   NO↓, 1,   VEGF↓, 5,   ZBTB10↑, 1,  

Barriers & Transport ⓘ

GLUT1↓, 2,  

Immune & Inflammatory Signaling ⓘ

COX1↓, 1,   COX2↓, 7,   CXCc↓, 1,   HCAR1↓, 1,   IL2↓, 1,   IL6↓, 1,   IL8↓, 1,   Imm↑, 3,   Inflam↓, 1,   JAK↓, 1,   JAK2↓, 2,   NF-kB↓, 20,   NK cell↑, 1,   p50↓, 1,   p65↓, 2,   PGE2↓, 1,   TNF-α↓, 1,  

Cellular Microenvironment ⓘ

pH↑, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 5,   BioAv↑, 7,   BioAv↝, 1,   ChemoSen↓, 1,   ChemoSen↑, 12,   Dose↑, 1,   Dose↝, 1,   eff↓, 4,   eff↑, 4,   Half-Life↓, 2,   RadioS↑, 7,   selectivity↑, 1,  

Clinical Biomarkers ⓘ

EGFR↓, 2,   EZH2↓, 1,   GutMicro↑, 1,   hTERT/TERT↓, 1,   IL6↓, 1,   TP53↑, 1,  

Functional Outcomes ⓘ

cachexia↓, 1,   cardioP↑, 3,   chemoP↑, 1,   hepatoP↑, 1,   neuroP↑, 1,   toxicity↓, 1,  
Total Targets: 194

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↓, 1,   antiOx↑, 8,   Catalase↑, 6,   Ferroptosis↓, 1,   GPx↑, 2,   GSH↑, 3,   GSR↓, 1,   GSTs↑, 2,   H2O2↓, 1,   HO-1↑, 4,   Keap1↓, 1,   lipid-P↓, 5,   MDA↓, 6,   MDA↑, 1,   NQO1↑, 1,   NRF2↓, 1,   NRF2↑, 7,   ROS↓, 14,   SOD↑, 6,   mt-SOD↑, 1,   TAC↑, 1,  

Metal & Cofactor Biology ⓘ

IronCh↑, 1,  

Mitochondria & Bioenergetics ⓘ

AIF↓, 1,   ATP↑, 1,  

Core Metabolism/Glycolysis ⓘ

ALAT↓, 1,   cytoP450↓, 1,   LDH↓, 1,   SIRT1↑, 1,  

Cell Death ⓘ

Apoptosis↓, 1,   Casp3↓, 1,   Casp9↓, 1,   CK2↑, 1,   Ferroptosis↓, 1,   iNOS↓, 1,  

Kinase & Signal Transduction ⓘ

Sp1/3/4↓, 2,  

Transcription & Epigenetics ⓘ

HATs↓, 1,   other↓, 1,  

DNA Damage & Repair ⓘ

P53↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

GSK‐3β↓, 2,   HDAC↑, 1,   neuroG↑, 1,   STAT↓, 1,  

Migration ⓘ

AP-1↓, 1,   miR-22↑, 1,  

Angiogenesis & Vasculature ⓘ

NO↓, 1,   NO↑, 2,  

Barriers & Transport ⓘ

BBB↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   COX2↑, 1,   ICAM-1↓, 1,   IL1↓, 1,   IL1β↓, 2,   IL2↓, 1,   IL4↓, 1,   IL6↓, 2,   INF-γ↓, 1,   Inflam↓, 12,   MCP1↓, 1,   NF-kB↓, 4,   PGE2↓, 1,   TLR2↓, 1,   TNF-α↓, 3,  

Synaptic & Neurotransmission ⓘ

AChE↓, 1,   ADAM10↑, 1,   tau↓, 3,  

Protein Aggregation ⓘ

Aβ↓, 6,   BACE↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 7,   BioAv↑, 8,   BioAv↝, 1,   eff↑, 1,   Half-Life↓, 2,  

Clinical Biomarkers ⓘ

ALAT↓, 1,   AST↓, 1,   IL6↓, 2,   LDH↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 1,   AntiTum↓, 1,   cardioP↑, 1,   cognitive↑, 4,   hepatoP↑, 3,   memory↑, 4,   neuroP↑, 2,   Obesity↓, 1,   radioP↑, 3,   toxicity↓, 1,   Wound Healing↑, 2,  
Total Targets: 87

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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