TGF-β Cancer Research Results

TGF-β, transforming growth factor-beta: Click to Expand ⟱
Source: HalifaxProj(inhibit) CGL-CS TCGA
Type:
Human malignancies frequently exhibit mutations in the TGF-β pathway, and overactivation of this system is linked to tumor growth by promoting angiogenesis and inhibiting the innate and adaptive antitumor immune responses.
Anti-inflammatory cytokine.
In normal tissues, TGF-β plays an essential role in cell cycle regulation, immune function, and tissue remodeling.
- In early carcinogenesis, TGF-β typically acts as a tumor suppressor by inhibiting cell proliferation and inducing apoptosis.

In advanced cancers, cells frequently become resistant to the growth-inhibitory effects of TGF-β.
- TGF-β then switches roles and promotes tumor progression by stimulating epithelial-to-mesenchymal transition (EMT), cell invasion, metastasis, and immune evasion.

Non-canonical (Smad-independent) pathways, such as MAPK, PI3K/Akt, and Rho signaling, also contribute to TGF-β-mediated responses.

Elevated levels of TGF-β have been detected in many advanced-stage cancers, including breast, lung, colorectal, pancreatic, and prostate cancers.
 - The switch from a tumor-suppressive to a tumor-promoting role is often associated with increased TGF-β production and activation in the tumor microenvironment.

High TGF-β expression or signaling activity is frequently correlated with aggressive disease features, resistance to therapy, increased metastasis, and poorer overall survival in many cancer types.
Thyroid, Thyroid: Click to Expand ⟱
Thyroid


Scientific Papers found: Click to Expand⟱
1124- ALA,    Alpha lipoic acid inhibits proliferation and epithelial mesenchymal transition of thyroid cancer cells
- in-vitro, Thyroid, BCPAP - in-vitro, Thyroid, HTH-83 - in-vitro, Thyroid, CAL-62 - in-vitro, Thyroid, FTC-133 - in-vivo, NA, NA
TumCP↓, AMPK↑, mTOR↓, TumCMig↓, TumCI↓, EMT↓, E-cadherin↑, β-catenin/ZEB1↓, Vim↓, Snail↓, Twist↓, TGF-β↓, p‑SMAD2↓, TumCG↓,
1072- EGCG,    Epigallocatechin gallate (EGCG) suppresses epithelial-Mesenchymal transition (EMT) and invasion in anaplastic thyroid carcinoma cells through blocking of TGF-β1/Smad signaling pathways
- in-vitro, Thyroid, 8505C
EMT↓, TumCI↓, TumCMig↓, TGF-β↓, p‑SMAD2↓, p‑SMAD3↓, SMAD4↓,

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:


Core Metabolism/Glycolysis ⓘ

AMPK↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

EMT↓, 2,   mTOR↓, 1,   TumCG↓, 1,  

Migration ⓘ

E-cadherin↑, 1,   p‑SMAD2↓, 2,   p‑SMAD3↓, 1,   SMAD4↓, 1,   Snail↓, 1,   TGF-β↓, 2,   TumCI↓, 2,   TumCMig↓, 2,   TumCP↓, 1,   Twist↓, 1,   Vim↓, 1,   β-catenin/ZEB1↓, 1,  
Total Targets: 16

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: TGF-β, transforming growth factor-beta
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:43  Cells:%  prod#:%  Target#:304  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

Home Page