Grapeseed extract / NF-kB 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.



NF-kB, Nuclear factor kappa B: Click to Expand ⟱
Source: HalifaxProj(inhibit)
Type:
NF-kB signaling
Nuclear factor kappa B (NF-κB) is a transcription factor that plays a crucial role in regulating immune response, inflammation, cell proliferation, and survival.
NF-κB is often found to be constitutively active in many types of cancer cells. This persistent activation can promote tumorigenesis by enhancing cell survival, proliferation, and metastasis.
Scientific Papers found: Click to Expand⟱
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 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:


Proliferation, Differentiation & Cell State ⓘ

EMT↓, 1,  

Migration ⓘ

E-cadherin↑, 1,   Fibronectin↓, 1,   N-cadherin↓, 1,   TumCI↓, 1,   TumCMig↓, 1,   Vim↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   NF-kB↓, 1,   PGE2↓, 1,  
Total Targets: 10

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: NF-kB, Nuclear factor kappa B
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#:214  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

 

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