GSK‐3β Cancer Research Results

GSK‐3β, Glycogen synthase kinase (GSK)3β: Click to Expand ⟱
Source:
Type:
GSK3β is a crucial member of the Wnt/β-catenin-, hedgehog (Hh)-, notch- and c-myc-mediated major pro-oncogenic pathways, while also being a negative regulator of epithelial–mesenchymal transition (EMT). Accumulating evidence defines GSK3β as a potential therapeutic target in cancer, thus encouraging the development of GSK3β inhibitors for cancer treatment.
Glycogen synthase kinase 3 beta (GSK-3β) is a serine/threonine kinase that plays a crucial role in various cellular processes, including cell proliferation, differentiation, and apoptosis. Its expression and activity have been implicated in several types of cancer, often with varying prognostic implications.

In many cancers, decreased GSK-3β activity is associated with poor prognosis, while in others, increased activity may correlate with aggressive disease.


Pca, Prostate Cancer: Click to Expand ⟱
Prostate Cancer: Alterations in genes such as ERG, SPOP, MYC, androgen receptor (AR), and CHD1, drive PCa progression.
TP53 is the most commonly mutated gene in human cancer.
HH↑, GLI-1↑, SHH↑ P53↓
The loss of p53 and/or other tumor suppressor genes, reduced capacity for DNA repair, the dysfunction of telomerase activity, and changes in the pathways that govern the growth of cells also mediate the progression of Pca.
It has been well documented that Ca2+ influx and MDR1 upregulation are highly associated with GEM metabolism in human pancreatic carcinoma.
Increased Growth factor IGF-1/IGF-1R axis activation mediated by both PI3K/Akt or RAF/MEK/ERK system and AR expression remains important in the development and progression of prostate cancer.
It has been demonstrated that prostate cancer cells are relatively sensitive to heat stress.
Long non-coding RNA MALAT1 has been reported as an oncogenic target in multiple types of cancers, including PC.
Scientific Papers found: Click to Expand⟱
1121- JG,    Juglone suppresses epithelial-mesenchymal transition in prostate cancer cells via the protein kinase B/glycogen synthase kinase-3β/Snail signaling pathway
- in-vitro, Pca, LNCaP
E-cadherin↑, N-cadherin↓, Vim↓, Snail↓, GSK‐3β↑,
5123- Sal,    Salinomycin suppresses LRP6 expression and inhibits both Wnt/β-catenin and mTORC1 signaling in breast and prostate cancer cells
- in-vitro, BC, MCF-7 - in-vitro, Pca, PC3 - in-vitro, Pca, DU145 - in-vitro, BC, MDA-MB-231 - in-vitro, Nor, HEK293
Wnt↓, β-catenin/ZEB1↓, mTORC1↓, GSK‐3β↑, cycD1/CCND1↓, survivin↓, LRP6↓, TumCG↓, Apoptosis↑,

Showing Research Papers: 1 to 2 of 2

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 2

Pathway results for Effect on Cancer / Diseased Cells:


Cell Death ⓘ

Apoptosis↑, 1,   survivin↓, 1,  

Cell Cycle & Senescence ⓘ

cycD1/CCND1↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

GSK‐3β↑, 2,   LRP6↓, 1,   mTORC1↓, 1,   TumCG↓, 1,   Wnt↓, 1,  

Migration ⓘ

E-cadherin↑, 1,   N-cadherin↓, 1,   Snail↓, 1,   Vim↓, 1,   β-catenin/ZEB1↓, 1,  
Total Targets: 13

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: GSK‐3β, Glycogen synthase kinase (GSK)3β
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:22  Cells:%  prod#:%  Target#:385  State#:%  Dir#:2
  wNotes=0  sortOrder:rid,rpid

 

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