Curcumin / TumCMig 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
TumCMig, Tumor cell migration: Click to Expand ⟱
Source:
Type:
Tumor cell migration is a critical process in cancer progression and metastasis, which is the spread of cancer cells from the primary tumor to distant sites in the body.
Scientific Papers found: Click to Expand⟱
147- ATG,  EGCG,  CUR,    Increased chemopreventive effect by combining arctigenin, green tea polyphenol and curcumin in prostate and breast cancer cells
- in-vitro, Pca, LNCaP - in-vitro, Pca, MCF-7
Bax:Bcl2↑, combination treatment significantly increased the ratio of Bax to Bcl-2 proteins, decreased the activation of NFκB, PI3K/Akt and Stat3
NF-kB↓, arctigenin demonstrated the strongest ability to inhibit the activation of both PI3K/Akt and NFκB pathways in both LNCaP and MCF-7 cells.
PI3K/Akt↓,
STAT3↓,
chemoPv↑, combining Arc and EGCG with Cur to enhance chemoprevention in both prostate and breast cancer.
TumCP↓, combining Arc and EGCG with Cur to enhance chemoprevention in both prostate and breast cancer.
TumCCA↑, EGCG significantly increased the effect of curcumin on cell cycle arrest at G0/G1 phase in MCF-7 cells, and the effect was further enhanced by the addition of arctigenin
TumCMig↓, EGCG and arctigenin alone or in combination with curcumin significantly decreased the number of migrated MCF-7 cells compared to control

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↓, Curcumin significantly inhibited migration and invasion in A549 cells, accompanied by significantly elevated miR-206 expression.
TumCI↓,
miR-206↑, Overexpression of miR-206 could inhibit migration and invasion of A549 cells, but it could also significantly decrease the phosphorylation levels of mTOR and AKT.
p‑mTOR↓,
p‑Akt↓,

4709- CUR,    Curcumin Regulates Cancer Progression: Focus on ncRNAs and Molecular Signaling Pathways
- Review, Var, NA
miR-21↓, Curcumin can effectively repress the miR-21/PTEN/Akt molecular pathway to inhibit cell proliferation and induce apoptosis in gastric cancer cells
TumCP↓, Curcumin can inhibit the proliferation, migration, invasion and promote apoptosis of retinoblastoma cells, which function through up-regulating the miR-99a expression and then inhibiting JAK/STAT signaling pathway
TumCMig↓,
TumCI↓,
Apoptosis↑,
miR-99↑,
JAK↓,
STAT↓,
cycD1/CCND1↓, curcumin can suppress the cell proliferation by down-regulations of cyclinD1 and up-regulations of p21 expression.
P21↑,
ChemoSen↑, curcumin combined with chemotherapy drugs may play a better therapeutic effect via JAK/STAT signaling pathway
miR-192-5p↑, curcumin enhanced the expression level of miR−192−5p and decreased the expression of c−Myc.
cMyc↓,
Wnt↓, curcumin suppresses colon cancer by inhibiting Wnt/β-catenin pathway via down-regulating miR-130a
β-catenin/ZEB1↓,
miR-130a↓,

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↓, Curcumin significantly inhibits cell migration, invasion, and colony formation in vitro and reduces tumor growth and liver metastasis in vivo.
TumCI↓,
TumCG↓,
TumMeta↓,
Sp1/3/4↓, curcumin suppresses Sp-1 transcriptional activity and Sp-1 regulated genes including ADEM10, calmodulin, EPHB2, HDAC4, and SEPP1 in CRC cells.
HDAC4↓,
FAK↓, Curcumin inhibits focal adhesion kinase (FAK) phosphorylation
CD24↓, Curcumin reduces CD24 expression in a dose-dependent manner in CRC cells
E-cadherin↑, E-cadherin expression is upregulated by curcumin and serves as an inhibitor of EMT.
EMT↓,
TumCP↓,
NF-kB↓, CUR prevents cancer cells migration, invasion, and metastasis through inhibition of PKC, FAK, NF-κB, p65, RhoA, MMP-2, and MMP-7 gene expressions
AP-1↝,
STAT3↓, downregulation of CD24 reduces STAT and FAK activity, decreases cell proliferation, metastasis in human tumor
P53?,
β-catenin/ZEB1↓, CUR could activate protein kinase D1 (PKD1) suggesting that suppressing of β-catenin transcriptional activity prevents growth of prostate cancer
NOTCH1↝,
Hif1a↝,
PPARα↝,
Rho↓, CUR prevents cancer cells migration, invasion, and metastasis through inhibition of PKC, FAK, NF-κB, p65, RhoA, MMP-2, and MMP-7 gene expressions
MMP2↓,
MMP9↓,

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↓, induced S phase cell cycle arrest
Apoptosis↑,
TumCCA↑,
Wnt↓,
EMT↓,
E-cadherin↑,
Vim↓,

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↑, inhibited cell cycle progression in G0/G1-S phase
Bcl-2↓,
CDK4/6↓, CDK4
cycD1/CCND1↓,

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↑,

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↓, Both mRNA and protein levels of SHH/GLI1 signaling (Shh, Smo, GLI1) were downregulated in a dose‐ and time‐dependent manner
Shh↓, inhibition of SHH/GLI1 signaling by curcumin may act as a novel mechanism of the apoptosis.
Gli1↓,
cycD1/CCND1↓,
Bcl-2↓,
FOXM1↓,
Bax:Bcl2↑, The Bax/Bcl‐2 ratio (Figure 6D) also gradually increased.
TumCP↓, Curcumin suppressed cell proliferation, colony formation, migration, and induced apoptosis which was mediated partly through the mitochondrial pathway after an increase in the ratio of Bax to Bcl2.
TumCMig↓,
Apoptosis↑,
TumVol↑, Intraperitoneal injection of curcumin in vivo reduced tumor volume,
TumCCA↑, Curcumin Inhibited Proliferation of Human Glioma Cells and induced G2/M Arrest
Casp3↑, level of caspase‐3 increases significantly after curcumin treatment.
OS↑, Curcumin Inhibited GBM Growth in Vivo through SHH/GLI1 Signaling and Prolonged the Survival Period

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↑,

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↓,

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↓, also cellular uptake of curcumin was significantly higher in CD44+ colon cancer cells.
CSCs↓, been suggested that curcumin was effective against colon CSCs by coupling with CD44

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↑,

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↑,

479- CUR,    Curcumin Has Anti-Proliferative and Pro-Apoptotic Effects on Tongue Cancer in vitro: A Study with Bioinformatics Analysis and in vitro Experiments
- in-vitro, Tong, CAL27
TumCP↓,
TumCMig↓,
Apoptosis↑,
TumCCA↑, S-phase cell cycle arrest
Bcl-2↓,
BAX↑,
cl‑Casp3↑,

480- CUR,    Curcumin exerts its tumor suppressive function via inhibition of NEDD4 oncoprotein in glioma cancer cells
- in-vitro, GBM, SNB19
TumCP↓,
TumCMig↓,
Apoptosis↑,
TumCCA↑, G2/M phase
NEDD9↓,
NOTCH1↓,
p‑Akt↓,

133- CUR,    Curcumin inhibits prostate cancer by targeting PGK1 in the FOXD3/miR-143 axis
- in-vitro, Pca, DU145 - in-vitro, Pca, PC3
miR-143↑, Curcumin treatment significantly upregulated miR-143 and decreased prostate cancer cell proliferation and migration.
PDK1↓, curcumin treatment inhibited PGK1 expression
FOXD3↑, Curcumin time-dependently upregulated FOXD3, which accounted for the escalating miR-143 levels with the duration of curcumin treatment.
TumCP↓, Furthermore, we showed that silencing miR-143 abrogated the effect of curcumin in inhibiting cell proliferation and migration.
TumCMig↓,
*Inflam↓, pharmaceutical properties of curcumin include antiinflammatory, antioxidant, chemo-preventative, and chemotherapeutic properties
*antiOx↑,
*chemoPv↑,
RadioS↑, underlying mechanism of curcumin in prostate cancer therapy, potentiating the clinical utility of curcumin as a chemo-preventive, chemotherapeutic, radio-, and drug-sensitizing agent.
ChemoSen↑,

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↓, suppression of the hedgehog signaling pathway
Shh↓, Curcumin significantly decreased hypoxia-induced expression levels of SHH, SMO and GLI1.
Smo↓,
Gli1↓,
N-cadherin↓,
E-cadherin↑,
Vim↓,
TumCP↓, inhibit the hypoxia-induced cell proliferation, migration and invasion in pancreatic cancer,
TumCMig↓,
TumCI↓,
EMT↓, mediate the expression of EMT-related factors.
chemoPv↑, Curcumin might be a potential candidate for chemoprevention of this severe disease.

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↓, MMP-9 activity is significantly inhibited by curcumin with less effect on MMP-2.
Matr↓, Fig. 2C, curcumin proficiently decreased the total levels of matriptase including latent matriptase (70kDa) and activated matriptase (a 120 kDa complex of activated matriptase and its cognate inhibitor HAI-1) in a dose-dependent manner.
Inflam↓, The antiinflammatory and antioxidant activities of curcumin have been proposed via inhibiting NF-kB,COX-2, iNOS, and cytokine production (9, 10).
antiOx↓,
NF-kB↓,
COX2↓,
iNOS↓,
TumCMig↓, Curcumin inhibition of prostate cancer cell migration and invasion
TumCI↓,

405- CUR,  5-FU,    Curcumin activates a ROS/KEAP1/NRF2/miR-34a/b/c cascade to suppress colorectal cancer metastasis
- vitro+vivo, CRC, HCT116
Apoptosis↑, more pronounced increase in apoptosis in p53-deficient when compared to p53-proficient cells
TumCMig↓,
NRF2↑,
ROS↑, antioxidant N-acetylcysteine suppressed the induction of apoptosis by curcumin
MET↑, Curcumin induces MET and inhibits lung-metastases formation via inducing miR-34a
miR-34a↑, Notably, curcumin induced miR-34a and miR-34b/c expression in a ROS/NRF2-dependent and p53-independent manner.

156- Ralox,  Tam,  GEN,  CUR,    Modulators of estrogen receptor inhibit proliferation and migration of prostate cancer cells
- in-vitro, Pca, DU145 - in-vitro, Pca, PC3
ERβ/ESR2↑,
TumCG↓, Regulation of PC cell growth by raloxifen, tamoxifen, genistein and curcumin
TumCMig↓, genistein and curcumin reduced the migratory activity of DU145 cells by 43% and 25%, respectively; for PC3 cells the reduction was about 40%
FAK↓, genistein seemed to be an inhibition of the activation of Focal Adhesion Kinase (FAK) and mitogen-activated kinase (MAPK) p38-heat shock protein 27 that mediates detachment and cellular migration respectively
p38↓,


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,   NRF2↑, 1,   ROS↑, 2,  

Mitochondria & Bioenergetics ⓘ

mtDam↑, 1,  

Core Metabolism/Glycolysis ⓘ

cMyc↓, 1,   IR↓, 1,   PDK1↓, 1,   PI3K/Akt↓, 1,   PPARα↝, 1,  

Cell Death ⓘ

p‑Akt↓, 3,   Apoptosis↑, 9,   BAX↑, 2,   Bax:Bcl2↑, 2,   Bcl-2↓, 5,   Casp3↓, 1,   Casp3↑, 2,   cl‑Casp3↑, 2,   iNOS↓, 1,   Myc↓, 1,   p38↓, 1,   β-TRCP↑, 1,  

Kinase & Signal Transduction ⓘ

FOXD3↑, 1,   Sp1/3/4↓, 1,  

Transcription & Epigenetics ⓘ

Matr↓, 1,   miR-143↑, 1,   miR-192-5p↑, 1,   miR-21↓, 1,   miR-30a-5p↑, 1,  

DNA Damage & Repair ⓘ

ATR↑, 1,   DNAdam↑, 1,   GADD45A↑, 1,   P53?, 1,   p‑P53↑, 1,   p73↑, 1,   PCLAF↓, 1,   p‑γH2AX↑, 1,  

Cell Cycle & Senescence ⓘ

cycD1/CCND1↓, 3,   P21↑, 2,   TumCCA↑, 6,  

Proliferation, Differentiation & Cell State ⓘ

CD24↓, 1,   CD44↓, 1,   CSCs↓, 1,   EMT↓, 5,   FOXM1↓, 2,   Gli1↓, 3,   HDAC4↓, 1,   HH↓, 2,   IGF-1↓, 1,   miR-34a↑, 2,   miR-99↑, 1,   p‑mTOR↓, 2,   NOTCH1↓, 1,   NOTCH1↝, 1,   PTEN↑, 1,   Shh↓, 3,   Smo↓, 1,   STAT↓, 1,   STAT3↓, 2,   TumCG↓, 3,   Wnt↓, 2,  

Migration ⓘ

AP-1↝, 1,   CDK4/6↓, 1,   E-cadherin↑, 5,   FAK↓, 2,   Galectin-9↓, 1,   MET↑, 1,   miR-130a↓, 1,   miR-206↑, 1,   MMP2↓, 1,   MMP9↓, 2,   N-cadherin↓, 2,   NEDD9↓, 2,   Rho↓, 1,   p‑SMAD2↓, 1,   p‑SMAD3↓, 1,   TGF-β↓, 1,   TumCI↓, 8,   TumCMig↓, 21,   TumCP↓, 13,   TumMeta↓, 1,   Vim↓, 2,   β-catenin/ZEB1↓, 3,  

Angiogenesis & Vasculature ⓘ

Hif1a↝, 1,  

Immune & Inflammatory Signaling ⓘ

CD25+↓, 1,   CD4+↓, 1,   COX2↓, 1,   FoxP3+↓, 1,   IFN-γ↑, 1,   Inflam↓, 1,   JAK↓, 1,   NF-kB↓, 3,   p‑p65↓, 1,   PD-1↓, 1,   PD-L1↓, 1,   PD-L2↓, 1,   T-Cell↑, 1,   TILs↑, 1,  

Cellular Microenvironment ⓘ

TIM-3↓, 1,  

Hormonal & Nuclear Receptors ⓘ

ERβ/ESR2↑, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 2,   RadioS↑, 1,  

Clinical Biomarkers ⓘ

FOXM1↓, 2,   Myc↓, 1,   PD-L1↓, 1,  

Functional Outcomes ⓘ

chemoPv↑, 2,   OS↑, 1,   TumVol↓, 1,   TumVol↑, 1,  

Infection & Microbiome ⓘ

CD8+↑, 1,  
Total Targets: 109

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,  

Immune & Inflammatory Signaling ⓘ

Inflam↓, 1,  

Functional Outcomes ⓘ

chemoPv↑, 1,  
Total Targets: 3

Scientific Paper Hit Count for: TumCMig, Tumor cell migration
21 Curcumin
1 Arctigenin
1 EGCG (Epigallocatechin Gallate)
1 Oxaliplatin
1 5-fluorouracil
1 raloxifen
1 tamoxifen
1 Genistein (soy isoflavone)
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#:326  State#:%  Dir#:%
  wNotes=on  sortOrder:rid,rpid

 

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