Curcumin / TumCI 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
TumCI, Tumor Cell invasion: Click to Expand ⟱
Source:
Type:
Tumor cell invasion is a critical process in cancer progression and metastasis, where cancer cells spread from the primary tumor to surrounding tissues and distant organs. This process involves several key steps and mechanisms:

1.Epithelial-Mesenchymal Transition (EMT): Many tumors originate from epithelial cells, which are typically organized in layers. During EMT, these cells lose their epithelial characteristics (such as cell-cell adhesion) and gain mesenchymal traits (such as increased motility). This transition is crucial for invasion.

2.Degradation of Extracellular Matrix (ECM): Tumor cells secrete enzymes, such as matrix metalloproteinases (MMPs), that degrade the ECM, allowing cancer cells to invade surrounding tissues. This degradation facilitates the movement of cancer cells through the tissue.

3.Cell Migration: Once the ECM is degraded, cancer cells can migrate. They often use various mechanisms, including amoeboid movement and mesenchymal migration, to move through the tissue. This migration is influenced by various signaling pathways and the tumor microenvironment.

4.Angiogenesis: As tumors grow, they require a blood supply to provide nutrients and oxygen. Tumor cells can stimulate the formation of new blood vessels (angiogenesis) through the release of growth factors like vascular endothelial growth factor (VEGF). This not only supports tumor growth but also provides a route for cancer cells to enter the bloodstream.

5.Invasion into Blood Vessels (Intravasation): Cancer cells can invade nearby blood vessels, allowing them to enter the circulatory system. This step is crucial for metastasis, as it enables cancer cells to travel to distant sites in the body.

6.Survival in Circulation: Once in the bloodstream, cancer cells must survive the immune response and the shear stress of blood flow. They can form clusters with platelets or other cells to evade detection.

7.Extravasation and Colonization: After traveling through the bloodstream, cancer cells can exit the circulation (extravasation) and invade new tissues. They may then establish secondary tumors (metastases) in distant organs.

8.Tumor Microenvironment: The surrounding microenvironment plays a significant role in tumor invasion. Factors such as immune cells, fibroblasts, and signaling molecules can either promote or inhibit invasion and metastasis.
Scientific Papers found: Click to Expand⟱
4710- CUR,    Curcumin inhibits migration and invasion of non-small cell lung cancer cells through up-regulation of miR-206 and suppression of PI3K/AKT/mTOR signaling pathway
- in-vitro, Lung, A549
TumCMig↓, TumCI↓, miR-206↑, p‑mTOR↓, p‑Akt↓,
4709- CUR,    Curcumin Regulates Cancer Progression: Focus on ncRNAs and Molecular Signaling Pathways
- Review, Var, NA
miR-21↓, TumCP↓, TumCMig↓, TumCI↓, Apoptosis↑, miR-99↑, JAK↓, STAT↓, cycD1/CCND1↓, P21↑, ChemoSen↑, miR-192-5p↑, cMyc↓, Wnt↓, β-catenin/ZEB1↓, miR-130a↓,
4656- CUR,  EGCG,    Curcumin and epigallocatechin gallate inhibit the cancer stem cell phenotype via down-regulation of STAT3-NFκB signaling
- in-vitro, BC, MDA-MB-231 - in-vitro, BC, MCF-7
CSCs↓, CD44↓, p‑STAT3↓, NF-kB↓, TumCI↓,
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↓,
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↑,
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↓,
6216- CUR,    Role of Turmeric and Curcumin in Prevention and Treatment of Chronic Diseases: Lessons Learned from Clinical Trials
- Review, Var, NA
TumCG↓, angioG↓, EMT↓, TumCI↓, TumMeta↓, *GutMicro↑, *BioAv↓, *HO-1↑, *ROS↓, *COX2↓, *iNOS↓, PKCδ↓, EGFR↓, NF-kB↓, cJun↓, cFos↓, cMyc↓, Akt↓, PI3K↓, CDK4↓, *TNF-α↓, *CRP↓, *IL6↓, MMP9↓, VEGF↓, JAK↓, STAT↓, IL1↓, IL2↓, IL6↓, IL8↓, IL12↓, MCP1↓, Apoptosis↑, ER Stress↑, 5LO↓, XO↓, *NRF2↑, *HO-1↑, *AChE↓, *neuroP↑, *glucose↓, *GLUT2↑, *GLUT3↑, *GLUT4↑, *GlucoseCon↑, *AMPK↑, *BMD↑, *MDA↓, *eff↑, eff↑, P53↑, BAX↑, DNAdam↑, Bcl-2↓, CSCs↓, ALDH↓, CD133↑,
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↓,
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↓,
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↓,
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↑,
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↑,
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↓,
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↑,
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↓,
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↑,
158- CUR,    Curcumin-targeting pericellular serine protease matriptase role in suppression of prostate cancer cell invasion, tumor growth, and metastasis
- vitro+vivo, Pca, LNCaP - in-vitro, Pca, PC3
MMP9↓, Matr↓, Inflam↓, antiOx↓, NF-kB↓, COX2↓, iNOS↓, TumCMig↓, TumCI↓,
181- CUR,    The effects of curcumin on the invasiveness of prostate cancer in vitro and in vivo
- vitro+vivo, Pca, DU145
MMP2↓, MMP9↓, TumCP↓, TumCI↓,

Showing Research Papers: 1 to 21 of 21

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 21

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

antiOx↓, 1,   Ferroptosis↑, 2,   GPx4↓, 1,   GSH↓, 2,   HO-1↑, 1,   Iron↑, 1,   lipid-P↑, 1,   MDA↑, 1,   NADH↓, 1,   NRF2↑, 2,   OXPHOS↓, 1,   ROS↑, 6,  

Mitochondria & Bioenergetics ⓘ

ATP↓, 1,   ETC↓, 1,   MMP↓, 2,  

Core Metabolism/Glycolysis ⓘ

AMPK↑, 2,   cMyc↓, 3,   FASN↓, 1,   G6PD↓, 1,   GLS↓, 1,   GlucoseCon↓, 1,   Glycolysis↓, 1,   HK2↓, 1,   lactateProd↑, 1,   LDHA↓, 1,   PDK1↓, 1,   PKM2↓, 1,   PPARα↝, 1,   SCD1↓, 1,   SREBP2↓, 1,   Warburg↓, 1,  

Cell Death ⓘ

Akt↓, 5,   p‑Akt↓, 3,   Apoptosis↑, 10,   BAX↑, 3,   Bcl-2↓, 4,   Bcl-xL↓, 1,   Casp↑, 2,   Casp3↓, 1,   Casp3↑, 2,   cl‑Casp3↑, 1,   Casp9↓, 1,   Casp9↑, 1,   Cyt‑c↑, 1,   Ferroptosis↑, 2,   iNOS↓, 2,   MAPK↓, 2,   Mcl-1↓, 1,   MCT1↓, 1,   miR-7641↓, 1,   survivin↓, 1,   TumCD↓, 1,   β-TRCP↑, 1,  

Kinase & Signal Transduction ⓘ

Sp1/3/4↓, 1,  

Transcription & Epigenetics ⓘ

cJun↓, 1,   HATs↓, 1,   Matr↓, 1,   miR-192-5p↑, 1,   miR-205↑, 1,   miR-21↓, 2,   miR-30a-5p↑, 1,   PhotoS↑, 2,   sonoS↑, 1,  

Protein Folding & ER Stress ⓘ

ER Stress↑, 2,   HSP70/HSPA5↓, 1,   e-HSP70/HSPA5↓, 1,  

Autophagy & Lysosomes ⓘ

Beclin-1↓, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 1,   DNMTs↓, 2,   p16↑, 1,   P53?, 1,   P53↑, 3,   p73↑, 1,   PARP↑, 1,   cl‑PARP↑, 1,   PCLAF↓, 1,  

Cell Cycle & Senescence ⓘ

CDK2↓, 1,   CDK4↓, 1,   CycB/CCNB1↓, 1,   cycD1/CCND1↓, 3,   P21↑, 1,   TumCCA↑, 4,  

Proliferation, Differentiation & Cell State ⓘ

ALDH↓, 1,   Axin2↑, 1,   CD133↑, 1,   CD24↓, 1,   CD44↓, 1,   cFos↓, 1,   CSCs↓, 2,   EMT↓, 4,   FOXO1↓, 1,   Gli1↓, 1,   GSK‐3β↓, 2,   HDAC↓, 2,   HDAC4↓, 1,   HH↓, 1,   miR-34a↑, 1,   miR-99↑, 1,   mTOR↓, 4,   p‑mTOR↓, 2,   NOTCH↓, 1,   NOTCH1↝, 1,   PI3K↓, 4,   PTEN↑, 2,   Shh↓, 1,   Smo↓, 1,   STAT↓, 3,   p‑STAT1↓, 1,   p‑STAT2↓, 1,   STAT3↓, 5,   p‑STAT3↓, 1,   TumCG↓, 4,   Wnt↓, 5,  

Migration ⓘ

5LO↓, 2,   AP-1↓, 1,   AP-1↝, 1,   CDK4/6↓, 1,   E-cadherin↑, 3,   FAK↓, 1,   Fibronectin↓, 1,   miR-130a↓, 1,   miR-206↑, 1,   miR-301a-3p↓, 1,   MMP2↓, 3,   MMP9↓, 5,   MMPs↓, 4,   N-cadherin↓, 2,   NEDD9↓, 1,   PKCδ↓, 1,   Rho↓, 1,   TumCI↓, 22,   TumCMig↓, 8,   TumCP↓, 10,   TumMeta↓, 8,   Vim↓, 2,   β-catenin/ZEB1↓, 7,  

Angiogenesis & Vasculature ⓘ

angioG↓, 4,   EGFR↓, 1,   Hif1a↓, 1,   Hif1a↝, 1,   VEGF↓, 3,  

Barriers & Transport ⓘ

GLUT1↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX1↓, 1,   COX2↓, 4,   IL1↓, 1,   IL12↓, 1,   IL2↓, 2,   IL6↓, 1,   IL8↓, 1,   Imm↑, 2,   Inflam↓, 2,   JAK↓, 3,   p‑JAK↓, 1,   p‑JAK2↓, 1,   p‑JAK3↓, 1,   MCP1↓, 1,   NF-kB↓, 10,   NK cell↑, 1,   PGE2↓, 1,   TLR4↓, 1,   TNF-α↓, 1,  

Protein Aggregation ⓘ

XO↓, 1,  

Hormonal & Nuclear Receptors ⓘ

AR↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 2,   BioAv↑, 2,   ChemoSen↑, 6,   eff↑, 4,   Half-Life↓, 1,   RadioS↑, 2,  

Clinical Biomarkers ⓘ

AR↓, 1,   EGFR↓, 1,   GutMicro↑, 1,   IL6↓, 1,  

Functional Outcomes ⓘ

cardioP↑, 2,   chemoP↑, 1,   chemoPv↑, 1,   hepatoP↑, 1,  
Total Targets: 177

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↓, 1,   antiOx↑, 1,   Catalase↑, 1,   GSTs↑, 1,   HO-1↑, 3,   lipid-P↓, 1,   MDA↓, 2,   NRF2↑, 2,   ROS↓, 4,   SOD↑, 1,  

Core Metabolism/Glycolysis ⓘ

AMPK↑, 1,   cytoP450↓, 1,   glucose↓, 1,   GlucoseCon↑, 1,   GLUT2↑, 1,  

Cell Death ⓘ

iNOS↓, 1,  

Barriers & Transport ⓘ

GLUT3↑, 1,   GLUT4↑, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   CRP↓, 1,   IL1↓, 1,   IL6↓, 2,   Inflam↓, 3,   TNF-α↓, 2,  

Synaptic & Neurotransmission ⓘ

AChE↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 2,   BioAv↑, 2,   eff↑, 1,   Half-Life↓, 1,  

Clinical Biomarkers ⓘ

BMD↑, 1,   CRP↓, 1,   GutMicro↑, 1,   IL6↓, 2,  

Functional Outcomes ⓘ

AntiTum↓, 1,   neuroP↑, 1,   radioP↑, 2,  
Total Targets: 36

Scientific Paper Hit Count for: TumCI, Tumor Cell invasion
21 Curcumin
1 EGCG (Epigallocatechin Gallate)
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#:324  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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