Vitexin / Raf Cancer Research Results

VT, Vitexin: Click to Expand ⟱
Features:

Vitexin - Apigenin-8-C-Glucoside

Alternative Names: Apigenin-8-C-glucoside, apigenin-8-C-β-D-glucopyranoside

Type: Flavone C-glycoside / apigenin derivative

Function: Vitexin is a naturally occurring C-glycosylated flavone in which glucose is attached to apigenin at the C-8 position. It exhibits antioxidant, anti-inflammatory, metabolic, cardiovascular, neuroprotective, and antiproliferative activities and can modulate pathways involving NF-κB, Nrf2/HO-1, MAPK, PI3K/AKT, AMPK, HIF-1α, apoptosis, and oxidative stress.

-see also IsoVitexin

Cancer: Preclinical studies indicate antiproliferative, pro-apoptotic, anti-migratory, anti-invasive, and anti-inflammatory effects across multiple cancer models. Reported mechanisms include modulation of PI3K/AKT, MAPK, NF-κB, HIF-1α, ROS, apoptosis, and cell-cycle signaling. Clinical anticancer efficacy has not been established.

Alzheimer's Disease: Preclinical evidence suggests neuroprotective activity through antioxidant and anti-inflammatory effects, reduction of neuronal injury, regulation of oxidative stress and mitochondrial function, and modulation of signaling pathways relevant to cognitive impairment and amyloid-associated neurotoxicity. Clinical efficacy for Alzheimer's disease has not been established.
Raf, RAF kinases: Click to Expand ⟱
Source:
Type:
RAF kinases (ARAF, BRAF and CRAF (also known as RAF1) constitute core components of the RAS-RAF-MEK-ERK signalling cascade (ERK signalling), a pathway that mediates signals from cell surface receptors to the nucleus to regulate cell growth, differentiation and survival.
The RAF family of kinases includes key activators of the pro-tumourigenic mitogen-activated protein kinase pathway. Hyperactivation of RAF proteins, particularly BRAF and CRAF, drives tumour progression and drug resistance in many types of cancer.
Scientific Papers found: Click to Expand⟱
7908- VT,    Vitexin isolated from Prosopis cineraria leaves induce apoptosis in K-562 leukemia cells via inhibition of the BCR-ABL-Ras-Raf pathway
- in-vitro, AML, NA
MMP↓, DNAdam↑, BCR↓, ABL1↓, HRAS↓, NRAS↓, KRAS↓, Raf↓, p38↑, BAX↑, Casp9↑,

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:


Mitochondria & Bioenergetics(tgid=3) ⓘ

ABL1↓, 1,   BCR↓, 1,   MMP↓, 1,   Raf↓, 1,  

Cell Death(tgid=5) ⓘ

BAX↑, 1,   Casp9↑, 1,   p38↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

DNAdam↑, 1,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

HRAS↓, 1,   NRAS↓, 1,  

Migration(tgid=13) ⓘ

KRAS↓, 1,  

Clinical Biomarkers(tgid=22) ⓘ

KRAS↓, 1,  
Total Targets: 12

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: Raf, RAF kinases
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#:462  Target#:480  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

 

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