Grapeseed extract / ZO-1 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.



ZO-1, Zonula occludens-1: Click to Expand ⟱
Source:
Type:
ZO-1 (Zonula occludens-1) is a protein that plays a crucial role in the formation and maintenance of tight junctions in epithelial cells. Tight junctions are essential for maintaining the integrity of epithelial barriers and regulating the passage of ions and molecules across the cell membrane.

In the context of cancer, ZO-1 has been implicated in several ways:

1.Loss of ZO-1 expression: Reduced or lost expression observed in various types of cancer.
2.Disruption of tight junctions: Cancer cells often exhibit disrupted tight junctions, which can lead to increased permeability and the loss of epithelial barrier function. ZO-1 is a key component of tight junctions, and its disruption can contribute to the development and progression of cancer.
3.Epithelial-to-mesenchymal transition (EMT): ZO-1 has been shown to play a role in regulating EMT, a process by which epithelial cells acquire a mesenchymal phenotype. EMT is a key event in the development of cancer metastasis, and ZO-1's role in regulating this process is an area of active research.
4.Tumor suppressor function: ZO-1 has been proposed to have tumor suppressor functions, and its loss or downregulation can contribute to the development of cancer. ZO-1's tumor suppressor functions may be related to its ability to regulate cell growth, apoptosis, and cell migration.

ZO-1 generally acts as a tumor suppressor by maintaining epithelial integrity. In many cancers, downregulation or mislocalization of ZO-1 is observed and is associated with a poorer prognosis due to the facilitation of EMT 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↓,

Showing Research Papers: 1 to 1 of 1

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 1

Pathway results for Effect on Cancer / Diseased Cells:


Cell Death ⓘ

p‑Akt↓, 1,   p‑p38↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

EMT↓, 1,   p‑ERK↓, 1,  

Migration ⓘ

E-cadherin↑, 1,   MMP2↓, 1,   MMP9↓, 1,   N-cadherin↓, 1,   Slug↓, 1,   p‑SMAD2↓, 1,   p‑SMAD3↓, 1,   TumCI↓, 1,   TumCMig↓, 1,   Vim↓, 1,   ZO-1↑, 1,  
Total Targets: 15

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: ZO-1, Zonula occludens-1
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#:674  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

 

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