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⟱
2312- CUR,    Dual Role of Reactive Oxygen Species and their Application in Cancer Therapy
- Review, Var, NA
ROS↑, PKM2↓,
2466- CUR,    Regulatory Effects of Curcumin on Platelets: An Update and Future Directions
- Review, Nor, NA
*AntiAg↑, *antiOx↑, *Inflam↓, *12LOX↑, COX1↓, COX2↓, MMP9↓, NF-kB↓,
2579- CUR,  ART/DHA,    Curcumin-Artemisinin Combination Therapy for Malaria
- in-vivo, NA, NA
OS↑, toxicity↓,
2654- CUR,    Oxidative Stress Inducers in Cancer Therapy: Preclinical and Clinical Evidence
- Review, Var, NA
ROS↑, Catalase↓, SOD1↓, GLO-I↓, NADPH↓, TumCCA↑, Apoptosis↑, Akt↓, ER Stress↑, JNK↑, STAT3↓, BioAv↑,
3574- CUR,    The effect of curcumin (turmeric) on Alzheimer's disease: An overview
- Review, AD, NA
*antiOx↑, *Inflam↓, *lipid-P↓, *cognitive↑, *memory↑, *Aβ↓, *COX2↓, *ROS↓, *AP-1↓, *NF-kB↓, *TNF-α↓, *IL1β↓, *SOD↑, *GSH↑, *HO-1↑, *IronCh↑, *BioAv↓, *Half-Life↝, *Dose↝, *BBB↑, *BioAv↑, *toxicity∅, *eff↑,
2808- CUR,    Iron chelation by curcumin suppresses both curcumin-induced autophagy and cell death together with iron overload neoplastic transformation
- in-vitro, Liver, HUH7
Ferritin↓, IronCh↑, TumAuto↑, Apoptosis↑, eff↝, Dose↝,
2809- CUR,    Comparative absorption of curcumin formulations
- in-vivo, Nor, NA
BioAv↑, BioAv↑, BioAv↑, BioAv↑, BioAv↑, BioAv↓, Half-Life↝,
2810- CUR,    Effect of curcuminoids on oxidative stress: A systematic review and meta-analysis of randomized controlled trials
- Review, Nor, NA
*SOD↑, *lipid-P↓, *GSH↑, *Catalase↑, *ROS↓,
2811- CUR,    Effect of Curcumin Supplementation During Radiotherapy on Oxidative Status of Patients with Prostate Cancer: A Double Blinded, Randomized, Placebo-Controlled Study
- Human, Pca, NA
*antiOx↑, radioP↑, RadioS∅, *TAC↑, *SOD↓,
2812- CUR,    Curcumin Induces High Levels of Topoisomerase I− and II−DNA Complexes in K562 Leukemia Cells
- in-vitro, AML, K562
TOP1↑, TOP2↑, eff↓,
2813- CUR,    Oxidative Metabolites of Curcumin Poison Human Type II Topoisomerases
- Review, NA, NA
TOP2↑,
2814- CUR,    Curcumin in Cancer and Inflammation: An In-Depth Exploration of Molecular Interactions, Therapeutic Potentials, and the Role in Disease Management
- Review, Var, NA
*BioAv↓, *Inflam↓, *antiOx↑, AntiCan↑, CK2↓, GSK‐3β↓, EGFR↓, TOP1↓, TOP2↓, NF-kB↓, COX2↓, CRP↓,
3576- CUR,    Protective Effects of Indian Spice Curcumin Against Amyloid-β in Alzheimer's Disease
- Review, AD, NA
*Inflam↓, *antiOx↑, *memory↑, *Aβ↓, *BBB↑, *cognitive↑, *tau↓, *LDL↓, *AChE↓, *IL1β↓, *IronCh↑, *neuroP↑, *BioAv↝, *PI3K↑, *Akt↑, *NRF2↑, *HO-1↑, *Ferritin↑, *HO-2↓, *ROS↓, *Ach↑, *GSH↑, *Bcl-2↑, *ChAT↑,
3857- CUR,    Alpha-Secretase ADAM10 Regulation: Insights into Alzheimer’s Disease Treatment
- Review, AD, NA
*Inflam↓, *antiOx↑, *IronCh↑, *BBB↑, *ADAM10↝,
3856- CUR,    Curcumin induces IL-6 receptor shedding via the ADAM10 proteinase
- in-vitro, AD, NA
*ADAM10↑, *Inflam↓,
3831- CUR,    Traditional Chinese Medicine: Role in Reducing β-Amyloid, Apoptosis, Autophagy, Neuroinflammation, Oxidative Stress, and Mitochondrial Dysfunction of Alzheimer’s Disease
- Review, AD, NA
*neuroP↑, *ROS↓, *Ca+2↓, *MMP↑,
3797- CUR,    Curcumin reverses cognitive deficits through promoting neurogenesis and synapse plasticity via the upregulation of PSD95 and BDNF in mice
- in-vitro, NA, NA
*cognitive↑, *BDNF↑, *PSD95↑, *memory↑,
3795- CUR,    Curcumin: A Golden Approach to Healthy Aging: A Systematic Review of the Evidence
- Review, AD, NA
*antiOx↑, *Inflam↓, *AntiAge↑, *AMPK↑, *SIRT1↑, *NF-kB↓, *mTOR↓, *NLRP3↓, *NADPH↓, *ROS↓, *COX2↓, *MCP1↓, *IL1β↓, *IL17↓, *IL23↓, *TNF-α↓, *MPO↓, *IL10↑, *lipid-P↓, *SOD↑, *Aβ↓, *p‑tau↓, *GSK‐3β↓, *CDK5↓, *TXNIP↓, *NRF2↑, *NQO1↑, *HO-1↑, *OS↑, *memory↑, *BDNF↑, *neuroP↑, *BACE↓, *AChE↓, *LDL↓,
3794- CUR,    Curcumin hybrid molecules for the treatment of Alzheimer's disease: Structure and pharmacological activities
- Review, AD, NA
*GSK‐3β↓, *CDK5↓, *p‑tau↓, *IronCh↑, *ROS↓, *HO-1↑, *SOD↑, *Catalase↑, *GSH↑, *TNF-α↓, *IL6↓, *IL12↓, *NRF2↑, *PPARγ↑, *IL4↑, *AChE↓, *Dose↝, *GutMicro↑,
3793- CUR,    Curcumin Downregulates GSK3 and Cdk5 in Scopolamine-Induced Alzheimer’s Disease Rats Abrogating Aβ40/42 and Tau Hyperphosphorylation
- in-vivo, AD, NA
*Aβ↓, *p‑tau↓, *GSK‐3β↓, *CDK5↓, *memory↑,
3760- CUR,  GI,  CAP,  RosA,  PI  Extending the lore of curcumin as dipteran Butyrylcholine esterase (BChE) inhibitor: A holistic molecular interplay assessment
*AChE↓, *other↓, *other↓, *other↓, *other↓, *other↓, *other↓,
3753- CUR,  Gala,    A Novel Galantamine–Curcumin Hybrid Inhibits Butyrylcholinesterase: A Molecular Dynamics Study
- Study, AD, NA
*BChE↓, *AChE↓, *Ach↑, *cognitive↑, *memory↑, *ROS↓, *Inflam↓, *NF-kB↓, *COX2?,
3752- CUR,    Revealing the molecular interplay of curcumin as Culex pipiens Acetylcholine esterase 1 (AChE1) inhibitor
- in-vivo, AD, NA
*AChE↓,
3751- CUR,  Gala,    A Novel Galantamine-Curcumin Hybrid as a Potential Multi-Target Agent against Neurodegenerative Disorders
- in-vivo, AD, NA
*AChE↓, *MDA↑, *GSH↑, *BBB↑,
3750- CUR,  PI,    Synergistic Effects of Curcumin and Piperine as Potent Acetylcholine and Amyloidogenic Inhibitors With Significant Neuroprotective Activity in SH-SY5Y Cells via Computational Molecular Modeling and in vitro Assay
- in-vitro, AD, SH-SY5Y
*AChE↓, *neuroP↑,
3748- CUR,  RES,  Hup,  Riv,  Gala  Natural acetylcholinesterase inhibitors: A multi-targeted therapeutic potential in Alzheimer's disease
- Review, AD, NA
*AChE↓, *Inflam↓, *Aβ↓, *cognitive↑, *ROS↓,
3590- CUR,    The Holy Grail of Curcumin and its Efficacy in Various Diseases: Is Bioavailability Truly a Big Concern?
- Review, Var, NA - Review, AD, NA
*BioAv↓, *BioAv↑, Dose↑, *Dose↝, *BBB↑, *cognitive↑, *BioAv↑,
3588- CUR,    The effect of curcumin on cognition in Alzheimer’s disease and healthy aging: A systematic review of pre-clinical and clinical studies
- Review, AD, NA
*cognitive↝, *BioAv↑, *Inflam↓, *COX2↓, *iNOS↓, *NF-kB↓, *TNF-α↓, *IL1↓, *IL2↓, *IL6↓, *IL8↓, *IL12↓, *ROS↓, *RNS↓, *antiOx↑, *BBB↑, *BioAv↓, *cognitive↑, *memory↑, *tau↓, *eff↑,
3585- CUR,    Nanoparticle encapsulation improves oral bioavailability of curcumin by at least 9-fold when compared to curcumin administered with piperine as absorption enhancer
- Study, NA, NA
*BioAv↑,
3578- CUR,  SIL,    Curcumin, but not its degradation products, in combination with silibinin is primarily responsible for the inhibition of colon cancer cell proliferation
- in-vitro, CRC, DLD1
eff↑, BioAv↓, TumCG↓,
3579- CUR,  AgNPs,    Metal–Curcumin Complexes in Therapeutics: An Approach to Enhance Pharmacological Effects of Curcumin
- Review, NA, NA
*IronCh↑, *BioAv↑, *antiOx↑, *Inflam↓, *BioAv↑, ROS↑, *neuroP↑, *eff↑,
3580- CUR,    Curcumin Acts as Post-protective Effects on Rat Hippocampal Synaptosomes in a Neuronal Model of Aluminum-Induced Toxicity
- in-vivo, AD, NA
*ROS↓, *Cyt‑c↓, *Casp3↓, *neuroP↑,
3581- CUR,    Curcumin Attenuated Neurotoxicity in Sporadic Animal Model of Alzheimer's Disease
- NA, AD, NA
*antiOx↑, *Inflam↓, *BBB↑, *NRF2↑, *NF-kB↓, *cognitive↑, *ROS↓, *MDA↓, *SOD↑, *Catalase↑, *INF-γ↓, *IL4↓, *memory↑, *TNF-α↓, *IL1β↓,
3577- CUR,    Oral curcumin for Alzheimer's disease: tolerability and efficacy in a 24-week randomized, double blind, placebo-controlled study
- Trial, AD, NA
*cognitive∅, *BioAv↑,
3586- CUR,  PI,    Influence of piperine on the pharmacokinetics of curcumin in animals and human volunteers
- in-vivo, NA, NA
*BioAv↑,
3582- CUR,  PI,    Therapeutic and Preventive Effects of Piperine and its Combination with Curcumin as a Bioenhancer Against Aluminum-Induced Damage in the Astrocyte Cells
*eff↑, *IL6↓, *TGF-β↓, *BioAv↑,
3583- CUR,    Curcumin: an orally bioavailable blocker of TNF and other pro-inflammatory biomarkers
- Review, Arthritis, NA
*TNF-α↓, *IL1β↓, *NF-kB↓, *PGE2↓, *COX2↓, *MMPs↓, *eff↑,
3584- CUR,    Curcumin in Health and Diseases: Alzheimer’s Disease and Curcumin Analogues, Derivatives, and Hybrids
*AChE↓, *Inflam↓, *antiOx↑, *Aβ↓, *ROS↓,
455- CUR,    Curcumin Affects Gastric Cancer Cell Migration, Invasion and Cytoskeletal Remodeling Through Gli1-β-Catenin
- in-vitro, GC, SGC-7901
Shh↓, Gli1↓, FOXM1↓, β-catenin/ZEB1↓, TumCMig↓, Apoptosis↑, TumCCA↑, Wnt↓, EMT↓, E-cadherin↑, Vim↓,
472- CUR,    Curcumin inhibits ovarian cancer progression by regulating circ-PLEKHM3/miR-320a/SMG1 axis
- vitro+vivo, Ovarian, SKOV3 - vitro+vivo, Ovarian, A2780S
TumCP↓, Apoptosis↑, PCNA↓, miR-320a↓, BAX↑, cl‑Casp3↑, circ‑PLEKHM3↑, SMG1↑,
456- CUR,    Curcumin Promoted miR-34a Expression and Suppressed Proliferation of Gastric Cancer Cells
- vitro+vivo, GC, SGC-7901
miR-34a↑, TumCP↓, TumCMig↓, TumCI↓, TumCCA↑, Bcl-2↓, CDK4/6↓, cycD1/CCND1↓,
457- CUR,    Curcumin regulates proliferation, autophagy, and apoptosis in gastric cancer cells by affecting PI3K and P53 signaling
- in-vitro, GC, SGC-7901 - in-vitro, GC, BGC-823
TumCP↓, Apoptosis↑, TumAuto↑, P53↑, PI3K↓, P21↑, p‑Akt↓, p‑mTOR↓, Bcl-2↓, Bcl-xL↓, LC3I↓, BAX↑, Beclin-1↑, cl‑Casp3↑, cl‑PARP↑, LC3II↑, ATG3↑, ATG5↑,
458- CUR,    Curcumin suppresses gastric cancer by inhibiting gastrin‐mediated acid secretion
- vitro+vivo, GC, SGC-7901
Casp3↑, Apoptosis↑, TumCP↓,
459- CUR,    Curcumin inhibits cell proliferation and motility via suppression of TROP2 in bladder cancer cells
- in-vitro, Bladder, T24/HTB-9 - in-vitro, Bladder, RT4
Trop2↓, Apoptosis↑, cycE1↓, p27↑, TumCCA↑,
460- CUR,    Curcumin Suppresses microRNA-7641-Mediated Regulation of p16 Expression in Bladder Cancer
- in-vitro, Bladder, T24/HTB-9 - in-vitro, Bladder, TCCSUP - in-vitro, Bladder, J82
miR-7641↓, p16↑, Apoptosis↑, TumCI↓,
461- CUR,    Curcumin inhibits prostate cancer progression by regulating the miR-30a-5p/PCLAF axis
- in-vitro, Pca, PC3 - in-vitro, Pca, DU145
TumCP↓, TumCMig↓, TumCI↓, Apoptosis↑, miR-30a-5p↑, PCLAF↓, Bcl-2↓, Casp3↓, BAX↑, cl‑Casp3↑,
462- CUR,    Curcumin promotes cancer-associated fibroblasts apoptosis via ROS-mediated endoplasmic reticulum stress
- in-vitro, Pca, PC3
Bcl-2↓, MMP↓, cl‑Casp3↑, BAX↑, BIM↑, p‑PARP↑, PUMA↑, p‑P53↑, ROS↑, p‑ERK↑, p‑eIF2α↑, CHOP↑, ATF4↑,
463- CUR,    Curcumin induces autophagic cell death in human thyroid cancer cells
- in-vitro, Thyroid, K1 - in-vitro, Thyroid, FTC-133 - in-vitro, Thyroid, BCPAP - in-vitro, Thyroid, 8505C
TumAuto↑, LC3II↑, Beclin-1↑, p‑p38↑, p‑JNK↑, p‑ERK↑, p62↓, p‑PDK1↓, p‑Akt↓, p‑p70S6↓, p‑PIK3R1↓, p‑S6↓, p‑4E-BP1↓,
464- CUR,    Curcumin inhibits the viability, migration and invasion of papillary thyroid cancer cells by regulating the miR-301a-3p/STAT3 axis
- in-vitro, Thyroid, BCPAP - in-vitro, Thyroid, TPC-1
TumCI↓, TumCI↓, MMP2↓, MMP9↓, EMT↓, STAT3↓, miR-301a-3p↓, STAT↓, N-cadherin↓, Vim↓, Fibronectin↓, p‑JAK↓, p‑JAK2↓, p‑JAK3↓, p‑STAT1↓, p‑STAT2↓, E-cadherin↑,
465- CUR,    Curcumin inhibits the growth of liver cancer by impairing myeloid-derived suppressor cells in murine tumor tissues
- vitro+vivo, Liver, HepG2 - vitro+vivo, Liver, HUH7 - vitro+vivo, Liver, MHCC-97H
TumCG↓, MDSCs↓, TLR4↓, NF-kB↓, IL6↓, IL1↓, PGE2↓, COX2↓, GM-CSF↓, angioG↓, VEGF↓, CD31↓, GM-CSF↓, α-SMA↓, p‑IKKα↓, MyD88↓,

Showing Research Papers: 101 to 150 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 ⓘ

Catalase↓, 1,   ROS↑, 4,   SOD1↓, 1,  

Metal & Cofactor Biology ⓘ

Ferritin↓, 1,   IronCh↑, 1,  

Mitochondria & Bioenergetics ⓘ

MMP↓, 1,  

Core Metabolism/Glycolysis ⓘ

GLO-I↓, 1,   NADPH↓, 1,   p‑PDK1↓, 1,   p‑PIK3R1↓, 1,   PKM2↓, 1,   p‑S6↓, 1,  

Cell Death ⓘ

Akt↓, 1,   p‑Akt↓, 2,   Apoptosis↑, 9,   BAX↑, 4,   Bcl-2↓, 4,   Bcl-xL↓, 1,   BIM↑, 1,   Casp3↓, 1,   Casp3↑, 1,   cl‑Casp3↑, 4,   CK2↓, 1,   JNK↑, 1,   p‑JNK↑, 1,   miR-7641↓, 1,   p27↑, 1,   p‑p38↑, 1,   PUMA↑, 1,  

Kinase & Signal Transduction ⓘ

p‑p70S6↓, 1,  

Transcription & Epigenetics ⓘ

miR-30a-5p↑, 1,  

Protein Folding & ER Stress ⓘ

CHOP↑, 1,   p‑eIF2α↑, 1,   ER Stress↑, 1,  

Autophagy & Lysosomes ⓘ

ATG3↑, 1,   ATG5↑, 1,   Beclin-1↑, 2,   LC3I↓, 1,   LC3II↑, 2,   p62↓, 1,   TumAuto↑, 3,  

DNA Damage & Repair ⓘ

p16↑, 1,   P53↑, 1,   p‑P53↑, 1,   p‑PARP↑, 1,   cl‑PARP↑, 1,   PCLAF↓, 1,   PCNA↓, 1,   SMG1↑, 1,  

Cell Cycle & Senescence ⓘ

cycD1/CCND1↓, 1,   cycE1↓, 1,   P21↑, 1,   TumCCA↑, 4,  

Proliferation, Differentiation & Cell State ⓘ

p‑4E-BP1↓, 1,   EMT↓, 2,   p‑ERK↑, 2,   FOXM1↓, 1,   Gli1↓, 1,   GSK‐3β↓, 1,   miR-34a↑, 1,   p‑mTOR↓, 1,   PI3K↓, 1,   circ‑PLEKHM3↑, 1,   Shh↓, 1,   STAT↓, 1,   p‑STAT1↓, 1,   p‑STAT2↓, 1,   STAT3↓, 2,   TOP1↓, 1,   TOP1↑, 1,   TOP2↓, 1,   TOP2↑, 2,   TumCG↓, 2,   Wnt↓, 1,  

Migration ⓘ

CD31↓, 1,   CDK4/6↓, 1,   E-cadherin↑, 2,   Fibronectin↓, 1,   miR-301a-3p↓, 1,   miR-320a↓, 1,   MMP2↓, 1,   MMP9↓, 2,   N-cadherin↓, 1,   Trop2↓, 1,   TumCI↓, 5,   TumCMig↓, 3,   TumCP↓, 5,   Vim↓, 2,   α-SMA↓, 1,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   ATF4↑, 1,   EGFR↓, 1,   VEGF↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX1↓, 1,   COX2↓, 3,   CRP↓, 1,   GM-CSF↓, 2,   p‑IKKα↓, 1,   IL1↓, 1,   IL6↓, 1,   p‑JAK↓, 1,   p‑JAK2↓, 1,   p‑JAK3↓, 1,   MDSCs↓, 1,   MyD88↓, 1,   NF-kB↓, 3,   PGE2↓, 1,   TLR4↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 2,   BioAv↑, 6,   Dose↑, 1,   Dose↝, 1,   eff↓, 1,   eff↑, 1,   eff↝, 1,   Half-Life↝, 1,   RadioS∅, 1,  

Clinical Biomarkers ⓘ

CRP↓, 1,   EGFR↓, 1,   Ferritin↓, 1,   FOXM1↓, 1,   IL6↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 1,   OS↑, 1,   radioP↑, 1,   toxicity↓, 1,  
Total Targets: 127

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 11,   Catalase↑, 3,   GSH↑, 5,   HO-1↑, 4,   HO-2↓, 1,   lipid-P↓, 3,   MDA↓, 1,   MDA↑, 1,   MPO↓, 1,   NQO1↑, 1,   NRF2↑, 4,   RNS↓, 1,   ROS↓, 12,   SOD↓, 1,   SOD↑, 5,   TAC↑, 1,  

Metal & Cofactor Biology ⓘ

Ferritin↑, 1,   IronCh↑, 5,  

Mitochondria & Bioenergetics ⓘ

MMP↑, 1,  

Core Metabolism/Glycolysis ⓘ

12LOX↑, 1,   AMPK↑, 1,   LDL↓, 2,   NADPH↓, 1,   PPARγ↑, 1,   SIRT1↑, 1,  

Cell Death ⓘ

Akt↑, 1,   Bcl-2↑, 1,   Casp3↓, 1,   Cyt‑c↓, 1,   iNOS↓, 1,  

Transcription & Epigenetics ⓘ

Ach↑, 2,   other↓, 6,  

Proliferation, Differentiation & Cell State ⓘ

GSK‐3β↓, 3,   mTOR↓, 1,   PI3K↑, 1,  

Migration ⓘ

AntiAg↑, 1,   AP-1↓, 1,   Ca+2↓, 1,   CDK5↓, 3,   MMPs↓, 1,   TGF-β↓, 1,   TXNIP↓, 1,  

Barriers & Transport ⓘ

BBB↑, 7,  

Immune & Inflammatory Signaling ⓘ

COX2?, 1,   COX2↓, 4,   IL1↓, 1,   IL10↑, 1,   IL12↓, 2,   IL17↓, 1,   IL1β↓, 5,   IL2↓, 1,   IL23↓, 1,   IL4↓, 1,   IL4↑, 1,   IL6↓, 3,   IL8↓, 1,   INF-γ↓, 1,   Inflam↓, 13,   MCP1↓, 1,   NF-kB↓, 6,   PGE2↓, 1,   TNF-α↓, 6,  

Synaptic & Neurotransmission ⓘ

AChE↓, 10,   ADAM10↑, 1,   ADAM10↝, 1,   BChE↓, 1,   BDNF↑, 2,   ChAT↑, 1,   PSD95↑, 1,   tau↓, 2,   p‑tau↓, 3,  

Protein Aggregation ⓘ

Aβ↓, 6,   BACE↓, 1,   NLRP3↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 4,   BioAv↑, 10,   BioAv↝, 1,   Dose↝, 3,   eff↑, 5,   Half-Life↝, 1,  

Clinical Biomarkers ⓘ

Ferritin↑, 1,   GutMicro↑, 1,   IL6↓, 3,  

Functional Outcomes ⓘ

AntiAge↑, 1,   cognitive↑, 8,   cognitive↝, 1,   cognitive∅, 1,   memory↑, 8,   neuroP↑, 6,   OS↑, 1,   toxicity∅, 1,  
Total Targets: 91

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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