Grapeseed extract / VEGF 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.

VEGF, Vascular endothelial growth factor: Click to Expand ⟱

Source: HalifaxProj (inhibit)

Type:

A signal protein produced by many cells that stimulates the formation of blood vessels. Vascular endothelial growth factor (VEGF) is a signal protein that plays a crucial role in angiogenesis, the process by which new blood vessels form from existing ones. This process is vital for normal physiological functions, such as wound healing and the menstrual cycle, but it is also a key factor in the growth and spread of tumors in cancer.
Because of its significant role in tumor growth and progression, VEGF has become a target for cancer therapies. Anti-VEGF therapies, such as monoclonal antibodies (e.g., bevacizumab) and small molecule inhibitors, aim to inhibit the action of VEGF, thereby reducing blood supply to tumors and limiting their growth. These therapies have been used in various types of cancer, including colorectal, lung, and breast cancer.

Scientific Papers found: Click to Expand⟱

1241-

GSE,

PACs,

Grape seed proanthocyanidins inhibit angiogenesis via the downregulation of both vascular endothelial growth factor and angiopoietin signaling

in-vitro,

Nor,

*VEGF↓, *MMP2↓, *MMP9↓, *p‑VEGFR2↓,

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:

Total Targets: 0

Pathway results for Effect on Normal Cells:

Migration ⓘ

MMP2↓, 1, MMP9↓, 1,

Angiogenesis & Vasculature ⓘ

VEGF↓, 1, p‑VEGFR2↓, 1,
Total Targets: 4

Scientific Paper Hit Count for: VEGF, Vascular endothelial growth factor

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