Curcumin / Vim Cancer Research Results

CUR, Curcumin: Click to Expand ⟱
Features:
Curcumin is the main active ingredient in Tumeric. 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).
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

Rank Pathway / Axis Cancer Cells Normal Cells Label Primary Interpretation Notes
1 NF-κB signaling ↓ NF-κB activation ↓ inflammatory NF-κB tone Driver Suppression of survival and inflammatory transcription NF-κB is a primary, repeatedly validated curcumin target explaining pleiotropic downstream effects
2 STAT3 signaling ↓ STAT3 phosphorylation / activity ↔ or mild suppression Driver Loss of pro-survival and proliferative signaling STAT3 inhibition contributes to growth arrest, apoptosis sensitization, and reduced cytokine signaling in tumors
3 Reactive oxygen species (ROS) ↑ ROS (dose- & context-dependent) ↓ ROS / buffered Conditional Driver Biphasic redox modulation Curcumin can act as a pro-oxidant in cancer cells with high basal stress while acting antioxidant in normal cells
4 Mitochondrial integrity / intrinsic apoptosis ↓ ΔΨm; ↑ caspase activation ↔ preserved Driver Execution of intrinsic apoptosis Mitochondrial dysfunction and caspase activation occur downstream of NF-κB/STAT3 and ROS effects
5 PI3K → AKT → mTOR axis ↓ AKT / ↓ mTOR ↔ or adaptive suppression Secondary Reduced growth and anabolic signaling AKT/mTOR inhibition contributes to growth suppression and autophagy induction in cancer cells
6 Autophagy ↑ autophagy (protective or pro-death) ↑ adaptive autophagy Secondary Stress adaptation vs cell death Autophagy may be cytoprotective or cooperate with apoptosis depending on context and dose
7 HIF-1α / VEGF hypoxia–angiogenesis axis ↓ HIF-1α; ↓ VEGF ↔ minimal effect Secondary Anti-angiogenic pressure Suppression of hypoxia-driven transcription limits angiogenesis and tumor adaptation
8 Cell cycle regulation ↑ G2/M or G1 arrest ↔ largely spared Phenotypic Cytostatic growth control Cell-cycle arrest reflects upstream signaling and epigenetic effects rather than direct CDK inhibition
9 Migration / invasion (EMT, MMP axis) ↓ migration & invasion ↔ Phenotypic Anti-metastatic phenotype Reduced EMT markers and protease activity limit invasive behavior
10 Epigenetic regulation (p300/CBP HAT activity) ↓ histone acetylation ↔ modest Secondary Transcriptional reprogramming Curcumin modulates chromatin via HAT inhibition rather than classic HDAC inhibition


Vim, Vimentin: Click to Expand ⟱
Source:
Type:
Vimentin, a major constituent of the intermediate filament family of proteins, is ubiquitously expressed in normal mesenchymal cells and is known to maintain cellular integrity and provide resistance against stress. Vimentin is overexpressed in various epithelial cancers, including prostate cancer, gastrointestinal tumors, tumors of the central nervous system, breast cancer, malignant melanoma, and lung cancer. Vimentin’s overexpression in cancer correlates well with accelerated tumor growth, invasion, and poor prognosis; however, the role of vimentin in cancer progression remains obscure.

In many epithelial-derived tumors (carcinomas), elevated Vimentin expression is often observed in cancer cells that have undergone EMT. This upregulation is characteristic of a shift toward a mesenchymal state, which is associated with reduced cell–cell adhesion and increased motility. Vimentin expression is also noted in the tumor stroma, reflecting the presence and activation of mesenchymal cells such as cancer-associated fibroblasts (CAFs). This dual expression can contribute to the remodeling of the tumor microenvironment.
The degree of Vimentin expression may vary depending on the tumor type, grade, and stage. More aggressive and advanced tumors tend to show higher levels of Vimentin expression.

High Vimentin expression has been correlated with poor clinical outcomes in several cancers, including breast, colorectal, prostate, and lung cancers.
Elevated Vimentin levels are typically associated with higher tumor grade, increased invasiveness, enhanced metastatic potential, and a greater risk of recurrence.
As a component of the EMT signature, high Vimentin expression can serve as an indicator of a more aggressive tumor phenotype and is often associated with reduced overall survival.
- vimentin up-regulation is often used as a marker of EMT in cancer



Scientific Papers found: Click to Expand⟱
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↓,
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↑,
470- CUR,    Regulation of carcinogenesis and modulation through Wnt/β-catenin signaling by curcumin in an ovarian cancer cell line
- in-vitro, Ovarian, SKOV3
Wnt/(β-catenin)↓, EMT↓, DNMT3A↓, cycD1/CCND1↓, cMyc↓, Fibronectin↓, Vim↓, E-cadherin↑, SFRP5↑,
433- CUR,    Curcumin Inhibits the Migration and Invasion of Non-Small-Cell Lung Cancer Cells Through Radiation-Induced Suppression of Epithelial-Mesenchymal Transition and Soluble E-Cadherin Expression
- in-vitro, Lung, A549
E-cadherin↓, Vim↓, Slug↓, N-cadherin↓, Snail↓, MMP9↓, EMT↓,
443- CUR,    Reduced Caudal Type Homeobox 2 (CDX2) Promoter Methylation Is Associated with Curcumin’s Suppressive Effects on Epithelial-Mesenchymal Transition in Colorectal Cancer Cells
- in-vitro, CRC, SW480
DNMT1↓, DNMT3A↓, N-cadherin↓, Vim↓, Wnt↓, Snail↓, Twist↓, β-catenin/ZEB1↓, E-cadherin↑, EMT↓, CDX2↓,
442- CUR,  5-FU,    Curcumin may reverse 5-fluorouracil resistance on colonic cancer cells by regulating TET1-NKD-Wnt signal pathway to inhibit the EMT progress
- in-vitro, CRC, HCT116
Apoptosis↑, TumCP↓, TumCCA↑, TET1↑, NKD2↑, Wnt↓, EMT↓, Vim↑, E-cadherin↓, β-catenin/ZEB1↓, TCF↓, AXIN1↓,
478- CUR,    Curcumin decreases epithelial‑mesenchymal transition by a Pirin‑dependent mechanism in cervical cancer cells
- in-vitro, Cerv, SiHa
EMT↓, N-cadherin↓, Vim↓, Slug↓, Zeb1↓, PIR↓, Pirin↓, E-cadherin↑,
473- CUR,    Curcumin inhibits epithelial-mesenchymal transition in oral cancer cells via c-Met blockade
- in-vitro, Oral, HSC4 - in-vitro, Oral, Ca9-22
Vim↓, p‑cMET↓, p‑ERK↓, pro‑MMP9↓, E-cadherin↑,
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↑,
420- CUR,    Anti-metastasis activity of curcumin against breast cancer via the inhibition of stem cell-like properties and EMT
- in-vitro, BC, MCF-7 - in-vitro, BC, MDA-MB-231
Vim↓, Fibronectin↓, β-catenin/ZEB1↓, E-cadherin↓, CD44↑, CD24↓, OCT4↓, Nanog↓, SOX2↓,
424- CUR,    Curcumin inhibits autocrine growth hormone-mediated invasion and metastasis by targeting NF-κB signaling and polyamine metabolism in breast cancer cells
- in-vitro, BC, MCF-7 - in-vitro, BC, MDA-MB-231
Src↓, p‑STAT1↓, p‑Akt↓, p‑p44↓, p‑p42↓, RAS↓, Raf↓, Vim↓, β-catenin/ZEB1↓, P53↓, Bcl-2↓, Mcl-1↓, PIAS-3↑, SOCS-3↑, SOCS1↑, ROS↑, NF-kB↓, PAO↑, SSAT↑, P21↑, Bak↑,
429- CUR,    TAp63α Is Involved in Tobacco Smoke-Induced Lung Cancer EMT and the Anti-cancer Activity of Curcumin via miR-19 Transcriptional Suppression
- in-vitro, Lung, H1299 - in-vitro, Lung, A549
TAp63α↑, E-cadherin↑, ZO-1↑, Vim↓, N-cadherin↓, miR-19b↓,

Showing Research Papers: 1 to 12 of 12

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 12

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

PAO↑, 1,   ROS↑, 1,  

Mitochondria & Bioenergetics ⓘ

p‑p42↓, 1,   Raf↓, 1,  

Core Metabolism/Glycolysis ⓘ

cMyc↓, 1,   SSAT↑, 1,  

Cell Death ⓘ

p‑Akt↓, 1,   Apoptosis↑, 2,   Bak↑, 1,   Bcl-2↓, 1,   Mcl-1↓, 1,  

DNA Damage & Repair ⓘ

DNMT1↓, 1,   DNMT3A↓, 2,   P53↓, 1,  

Cell Cycle & Senescence ⓘ

cycD1/CCND1↓, 1,   P21↑, 1,   TAp63α↑, 1,   TumCCA↑, 2,  

Proliferation, Differentiation & Cell State ⓘ

AXIN1↓, 1,   CD24↓, 1,   CD44↑, 1,   CDX2↓, 1,   p‑cMET↓, 1,   EMT↓, 8,   p‑ERK↓, 1,   FOXM1↓, 1,   Gli1↓, 2,   HH↓, 1,   Nanog↓, 1,   NKD2↑, 1,   OCT4↓, 1,   PIAS-3↑, 1,   Pirin↓, 1,   RAS↓, 1,   SFRP5↑, 1,   Shh↓, 2,   Smo↓, 1,   SOX2↓, 1,   Src↓, 1,   STAT↓, 1,   p‑STAT1↓, 2,   p‑STAT2↓, 1,   STAT3↓, 1,   TCF↓, 1,   Wnt↓, 3,   Wnt/(β-catenin)↓, 1,  

Migration ⓘ

E-cadherin↓, 3,   E-cadherin↑, 8,   Fibronectin↓, 3,   miR-19b↓, 1,   miR-301a-3p↓, 1,   MMP2↓, 1,   MMP9↓, 2,   pro‑MMP9↓, 1,   N-cadherin↓, 6,   p‑p44↓, 1,   PIR↓, 1,   Slug↓, 2,   Snail↓, 2,   TET1↑, 1,   TumCI↓, 3,   TumCMig↓, 2,   TumCP↓, 2,   Twist↓, 1,   Vim↓, 11,   Vim↑, 1,   Zeb1↓, 1,   ZO-1↑, 1,   β-catenin/ZEB1↓, 5,  

Immune & Inflammatory Signaling ⓘ

p‑JAK↓, 1,   p‑JAK2↓, 1,   p‑JAK3↓, 1,   NF-kB↓, 1,   SOCS-3↑, 1,   SOCS1↑, 1,  

Clinical Biomarkers ⓘ

FOXM1↓, 1,  

Functional Outcomes ⓘ

chemoPv↑, 1,  
Total Targets: 77

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: Vim, Vimentin
12 Curcumin
1 5-fluorouracil
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#:336  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

 

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