Vim Cancer Research Results

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



Nor, Normal Healthy: Click to Expand ⟱
Normal Healthy
Scientific Papers found: Click to Expand⟱
1097- AG,    Astragalus Inhibits Epithelial-to-Mesenchymal Transition of Peritoneal Mesothelial Cells by Down-Regulating β-Catenin
- in-vitro, Nor, HMrSV5 - in-vivo, NA, NA
*EMT↓, *E-cadherin↑, *α-SMA↓, *Vim↓, *β-catenin/ZEB1↓, *Smad7↑,
2662- AL,    Allicin inhibits tubular epithelial-myofibroblast transdifferentiation under high glucose conditions in vitro
- in-vitro, Nor, HK-2
*α-SMA↓, *Vim↓, *COL1↓, *E-cadherin↑, *TGF-β1↓, *p‑ERK↓, *EMT↓,
2317- Api,    Apigenin intervenes in liver fibrosis by regulating PKM2-HIF-1α mediated oxidative stress
- in-vivo, Nor, NA
*hepatoP↑, *PKM2↓, *Hif1a↓, *MDA↓, *Catalase↓, *GSH↑, *SOD↑, *GPx↑, *TAC↑, *α-SMA↓, *Vim↓, *ROS↓,
1098- BA,    Baicalein inhibits fibronectin-induced epithelial–mesenchymal transition by decreasing activation and upregulation of calpain-2
- in-vitro, Nor, MCF10 - in-vivo, NA, NA
*TumCMig↓, *F-actin↓, *E-cadherin↑, *ZO-1↑, *N-cadherin↓, *Vim↓, *Snail↓, *cal2↓, *Ca+2↝,
2473- BA,    Baicalin Inhibits EMT through PDK1/AKT Signaling in Human Nonsmall Cell Lung Cancer
- in-vitro, Lung, A549 - in-vitro, Nor, BEAS-2B - in-vitro, Lung, H460
EMT↓, PDK1↓, Akt↓, TumCMig↓, E-cadherin↑, Vim↓,
2047- Buty,    Sodium butyrate inhibits migration and induces AMPK-mTOR pathway-dependent autophagy and ROS-mediated apoptosis via the miR-139-5p/Bmi-1 axis in human bladder cancer cells
- in-vitro, CRC, T24/HTB-9 - in-vitro, Nor, SV-HUC-1 - in-vitro, Bladder, 5637 - in-vivo, NA, NA
HDAC↓, AntiTum↑, TumCMig↓, AMPK↑, mTOR↑, TumAuto↑, ROS↑, miR-139-5p↑, BMI1↓, TumCI?, E-cadherin↑, N-cadherin↓, Vim↓, Snail↓, cl‑PARP↑, cl‑Casp3↑, BAX↑, Bcl-2↓, Bcl-xL↓, MMP↓, PINK1↑, PARK2↑, TumMeta↓, TumCG↓, LC3II↑, p62↓, eff↓,
3478- MF,    One Month of Brief Weekly Magnetic Field Therapy Enhances the Anticancer Potential of Female Human Sera: Randomized Double-Blind Pilot Study
- Trial, BC, NA - in-vitro, BC, MCF-7 - in-vitro, Nor, C2C12
TumCP↓, TumCMig↓, TumCI↓, *toxicity∅, TGF-β↓, Twist↓, Slug↓, β-catenin/ZEB1↓, Vim↓, p‑SMAD2↓, p‑SMAD3↓, angioG↓, VEGF↓, selectivity↑, LIF↑,
3048- SK,    Shikonin inhibits triple-negative breast cancer-cell metastasis by reversing the epithelial-to-mesenchymal transition via glycogen synthase kinase 3β-regulated suppression of β-catenin signaling
- in-vitro, BC, MDA-MB-231 - in-vitro, BC, 4T1 - in-vitro, Nor, MCF12A - in-vivo, NA, NA
tumCV↓, selectivity↑, EMT↓, TumCMig↓, TumCI↓, E-cadherin↑, N-cadherin↓, Vim↓, Snail↓, β-catenin/ZEB1↓, GSK‐3β↑,
1821- VitK3,    Menadione (Vitamin K3) induces apoptosis of human oral cancer cells and reduces their metastatic potential by modulating the expression of epithelial to mesenchymal transition markers and inhibiting migration
- in-vitro, Oral, NA - in-vitro, Nor, HEK293 - in-vitro, Nor, HaCaT
selectivity↑, TumCD↓, BAX↑, P53↑, Bcl-2↓, p65↓, E-cadherin↑, EMT↓, Vim↓, Fibronectin↓, TumCG↓, TumCMig↓,

Showing Research Papers: 1 to 9 of 9

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 9

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

PARK2↑, 1,   ROS↑, 1,  

Mitochondria & Bioenergetics ⓘ

MMP↓, 1,   PINK1↑, 1,  

Core Metabolism/Glycolysis ⓘ

AMPK↑, 1,   PDK1↓, 1,  

Cell Death ⓘ

Akt↓, 1,   BAX↑, 2,   Bcl-2↓, 2,   Bcl-xL↓, 1,   cl‑Casp3↑, 1,   TumCD↓, 1,  

Transcription & Epigenetics ⓘ

tumCV↓, 1,  

Autophagy & Lysosomes ⓘ

LC3II↑, 1,   p62↓, 1,   TumAuto↑, 1,  

DNA Damage & Repair ⓘ

P53↑, 1,   cl‑PARP↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

BMI1↓, 1,   EMT↓, 3,   GSK‐3β↑, 1,   HDAC↓, 1,   mTOR↑, 1,   TumCG↓, 2,  

Migration ⓘ

E-cadherin↑, 4,   Fibronectin↓, 1,   miR-139-5p↑, 1,   N-cadherin↓, 2,   Slug↓, 1,   p‑SMAD2↓, 1,   p‑SMAD3↓, 1,   Snail↓, 2,   TGF-β↓, 1,   TumCI?, 1,   TumCI↓, 2,   TumCMig↓, 5,   TumCP↓, 1,   TumMeta↓, 1,   Twist↓, 1,   Vim↓, 5,   β-catenin/ZEB1↓, 2,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   VEGF↓, 1,  

Immune & Inflammatory Signaling ⓘ

LIF↑, 1,   p65↓, 1,  

Drug Metabolism & Resistance ⓘ

eff↓, 1,   selectivity↑, 3,  

Functional Outcomes ⓘ

AntiTum↑, 1,  
Total Targets: 48

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

Catalase↓, 1,   GPx↑, 1,   GSH↑, 1,   MDA↓, 1,   ROS↓, 1,   SOD↑, 1,   TAC↑, 1,  

Core Metabolism/Glycolysis ⓘ

PKM2↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

EMT↓, 2,   p‑ERK↓, 1,  

Migration ⓘ

Ca+2↝, 1,   cal2↓, 1,   COL1↓, 1,   E-cadherin↑, 3,   F-actin↓, 1,   N-cadherin↓, 1,   Smad7↑, 1,   Snail↓, 1,   TGF-β1↓, 1,   TumCMig↓, 1,   Vim↓, 4,   ZO-1↑, 1,   α-SMA↓, 3,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature ⓘ

Hif1a↓, 1,  

Functional Outcomes ⓘ

hepatoP↑, 1,   toxicity∅, 1,  
Total Targets: 27

Scientific Paper Hit Count for: Vim, Vimentin
2 Baicalin
1 Astragalus
1 Allicin (mainly Garlic)
1 Apigenin (mainly Parsley)
1 Butyrate
1 Magnetic Fields
1 Shikonin
1 VitK3,menadione
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:49  Cells:%  prod#:%  Target#:336  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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