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.
PC, Pancreatic Cancer: Click to Expand ⟱
Pancreatic Cancer: Hypoxia (low oxygen tension) is commonly found in solid tumors. Hypoxia-inducible factor-1 (HIF-1),is a key mediator of the cellular response to hypoxia and is overexpressed in a wide variety of solid tumors, including pancreatic cancer.
Nanog is highly expressed in CSCs compared to normal cells [93–97]
HIF-1↑
Scientific Papers found: Click to Expand⟱
5280- 3BP,    Anticancer Efficacy of the Metabolic Blocker 3-Bromopyruvate: Specific Molecular Targeting
- in-vitro, PC, NA
mtDam↑, HK2↓, TGF-β↓, Casp3↑, selectivity↑,
4520- MAG,    Magnolol Suppresses Pancreatic Cancer Development In Vivo and In Vitro via Negatively Regulating TGF-β/Smad Signaling
- vitro+vivo, PC, PANC1
Vim↓, E-cadherin↑, EMT↓, N-cadherin↓, p‑SMAD2↓, p‑SMAD3↓, TumCP↓, TumCMig↓, TumCI↓, TGF-β↓,

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:


Mitochondria & Bioenergetics ⓘ

mtDam↑, 1,  

Core Metabolism/Glycolysis ⓘ

HK2↓, 1,  

Cell Death ⓘ

Casp3↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

EMT↓, 1,  

Migration ⓘ

E-cadherin↑, 1,   N-cadherin↓, 1,   p‑SMAD2↓, 1,   p‑SMAD3↓, 1,   TGF-β↓, 2,   TumCI↓, 1,   TumCMig↓, 1,   TumCP↓, 1,   Vim↓, 1,  

Drug Metabolism & Resistance ⓘ

selectivity↑, 1,  
Total Targets: 14

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:21  Cells:%  prod#:%  Target#:304  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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