Vitexin / HRAS 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.
HRAS, v-Ha-ras Harvey rat sarcoma viral oncogene homolog: Click to Expand ⟱
Source: CGL-Driver Genes
Type: Oncogene
HRAS (Harvey rat sarcoma viral oncogene homolog) is one of the three main RAS genes (HRAS, KRAS, and NRAS) that encode proteins involved in cell signaling pathways that control cell growth and differentiation. Mutations in HRAS can lead to uncontrolled cell proliferation and are associated with various types of cancer.
When mutated, HRAS can become constitutively active, leading to continuous signaling for cell division and survival, contributing to tumorigenesis.
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: HRAS, v-Ha-ras Harvey rat sarcoma viral oncogene homolog
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#:147  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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