Ginkgolic acids / PTEN Cancer Research Results

GAs, Ginkgolic acids: Click to Expand ⟱
Features:

Ginkgolic acids (GAs) are a group of naturally occurring 2-hydroxy-6-alkylsalicylic acids found in Ginkgo biloba leaves, seeds and especially the seed coat. Major congeners include ginkgolic acid C13:0, C15:1 and C17:1. Ginkgolic acids have demonstrated antimicrobial, antiviral, autophagy-modulating and anticancer activities in preclinical studies. In cancer models, GAs can suppress proliferation, migration and invasion and promote apoptosis through mechanisms including inhibition of SUMOylation, STAT3 signalling, Hsp90 activity and other oncogenic pathways. Individual congeners can differ substantially in potency and biological activity, so specific forms such as C15:1 or C17:1 should be recorded separately when identified. Ginkgolic acids are kept separate from standardized Ginkgo biloba extracts because they are considered potentially toxic constituents and are deliberately reduced to very low concentrations in purified medicinal ginkgo preparations. Current anticancer evidence is predominantly preclinical.



PTEN, phosphatase and tensin homolog; phosphatase and tensin homolog pseudogene 1: Click to Expand ⟱
Source: CGL-Driver Genes
Type: TSG
PTEN (Phosphatase and Tensin Homolog) is a crucial tumor suppressor gene that plays a significant role in regulating cell growth, proliferation, and survival. It encodes a protein that functions as a phosphatase, which means it removes phosphate groups from specific molecules, thereby regulating various signaling pathways, particularly the PI3K/AKT pathway.
PTEN is mutated, deleted, or otherwise inactivated. This loss of function can lead to increased cell proliferation and survival, contributing to tumorigenesis. PTEN mutations are commonly found in various cancers, including:
Prostate cancer
Breast cancer
Endometrial cancer
Glioblastoma


Scientific Papers found: Click to Expand⟱
1187- GAs,    Ginkgolic Acid C 17:1, Derived from Ginkgo biloba Leaves, Suppresses Constitutive and Inducible STAT3 Activation through Induction of PTEN and SHP-1 Tyrosine Phosphatase
- in-vitro, Melanoma, U251 - in-vitro, Melanoma, MM.1S
STAT3↓, PTEN↑, Apoptosis↑, PTPN6↑,

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(tgid=5)

Apoptosis↑, 1,  

Proliferation, Differentiation & Cell State(tgid=12)

PTEN↑, 1,   PTPN6↑, 1,   STAT3↓, 1,  
Total Targets: 4

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: PTEN, phosphatase and tensin homolog; phosphatase and tensin homolog pseudogene 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#:436  Target#:267  State#:%  Dir#:2
wNotes=0 sortOrder:rid,rpid

 

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