Grapeseed extract / Vim Cancer Research Results

GSE, Grapeseed extract: Click to Expand ⟱
Features:
Grapeseed extract (GSE) is rich in oligomeric proanthocyanidins (OPCs), catechins, and other polyphenols derived from Vitis vinifera seeds. In cancer research, GSE is most consistently associated with antioxidant and anti-inflammatory signaling modulation, suppression of PI3K/AKT and MAPK pathways, induction of cell-cycle arrest, and promotion of apoptosis in preclinical models. GSE has also been reported to inhibit angiogenesis (via VEGF suppression), reduce metastasis-related markers (e.g., MMPs), and modulate redox balance in tumor cells. Effects are concentration-dependent and vary by tumor type. While GSE is frequently described as antioxidant in normal tissues, pro-oxidant effects have been reported in tumor contexts at higher concentrations. Human oncology data remain limited; most findings derive from in vitro and animal studies.
Made from seeds of grapes and contains antioxidants Vitamin E, linolenic acid and OPCs.


Cancer Pathway Table: Grapeseed Extract

Rank Pathway / Axis Cancer / Tumor Context Normal Tissue Context TSF Primary Effect Notes / Interpretation
1 NF-κB inflammatory / survival signaling NF-κB ↓; COX-2 ↓; cytokines ↓ (reported) Inflammatory tone ↓ R, G Anti-inflammatory / anti-survival Consistent suppression of inflammatory signaling in multiple tumor models.
2 PI3K → AKT → mTOR axis PI3K/AKT ↓; proliferation ↓ (model-dependent) ↔ R, G Growth signaling suppression Frequently reported mechanism contributing to reduced tumor growth.
3 Intrinsic apoptosis (mitochondrial pathway) Bax ↑; Bcl-2 ↓; caspases ↑ (reported) Minimal apoptosis at lower exposure G Apoptotic induction Apoptosis induction associated with mitochondrial depolarization and cytochrome c release.
4 Cell-cycle arrest (G1 / G2-M) Cell-cycle arrest ↑ (reported) ↔ G Cytostasis Often linked to decreased Cyclin D1/CDK expression.
5 ROS modulation (biphasic) ROS ↑ in some tumor contexts; apoptosis ↑ ROS ↓; antioxidant protection P, R Redox modulation Polyphenol-rich extracts may act antioxidant in normal cells and pro-oxidant in tumor cells at higher doses.
6 Nrf2 / ARE pathway Context-dependent modulation Nrf2 ↑; antioxidant enzyme expression ↑ R, G Redox regulation Common polyphenol signature; may protect normal tissue during oxidative stress.
7 MAPK signaling (ERK / JNK / p38) Stress-MAPK modulation (context-dependent) ↔ P, R, G Signal reprogramming JNK/p38 activation linked to apoptosis; ERK modulation varies.
8 Angiogenesis (VEGF signaling) VEGF ↓; angiogenesis ↓ (reported) ↔ G Anti-angiogenic Anti-angiogenic activity observed in several preclinical systems.
9 Metastasis / invasion (MMPs) MMP2/MMP9 ↓; migration ↓ (reported) ↔ G Anti-invasive phenotype Likely downstream of NF-κB and MAPK suppression.
10 Bioavailability constraint Systemic exposure limited; metabolite-driven effects Generally well tolerated — Translation constraint OPCs have limited oral bioavailability; many in vitro concentrations exceed typical plasma levels.

TSF: P = rapid redox effects; R = signaling pathway modulation; G = apoptosis, angiogenesis, and phenotype-level changes.



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⟱
1118- GSE,    Grape Seed Proanthocyanidins Inhibit Migration and Invasion of Bladder Cancer Cells by Reversing EMT through Suppression of TGF- β Signaling Pathway
- in-vitro, Bladder, T24/HTB-9 - in-vitro, Bladder, 5637
TumCMig↓, TumCI↓, MMP2↓, MMP9↓, EMT↓, N-cadherin↓, Vim↓, Slug↓, E-cadherin↑, ZO-1↑, p‑SMAD2↓, p‑SMAD3↓, p‑Akt↓, p‑ERK↓, p‑p38↓,
1240- GSE,  PACs,    Grape Seed Proanthocyanidins Inhibit Melanoma Cell Invasiveness by Reduction of PGE2 Synthesis and Reversal of Epithelial-to-Mesenchymal Transition
- in-vitro, Melanoma, A375 - in-vitro, Melanoma, Hs294T
TumCMig↓, TumCI↓, COX2↓, PGE2↓, NF-kB↓, EMT↓, E-cadherin↑, Vim↓, Fibronectin↓, N-cadherin↓,

Showing Research Papers: 1 to 2 of 2

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 2

Pathway results for Effect on Cancer / Diseased Cells:


Cell Death ⓘ

p‑Akt↓, 1,   p‑p38↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

EMT↓, 2,   p‑ERK↓, 1,  

Migration ⓘ

E-cadherin↑, 2,   Fibronectin↓, 1,   MMP2↓, 1,   MMP9↓, 1,   N-cadherin↓, 2,   Slug↓, 1,   p‑SMAD2↓, 1,   p‑SMAD3↓, 1,   TumCI↓, 2,   TumCMig↓, 2,   Vim↓, 2,   ZO-1↑, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   NF-kB↓, 1,   PGE2↓, 1,  
Total Targets: 19

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: Vim, Vimentin
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#:91  Target#:336  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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