Grapeseed extract / TumCI 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.



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⟱
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: TumCI, Tumor Cell invasion
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#:324  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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