PDGFRA Cancer Research Results

PDGFRA, platelet-derived growth factor receptor, alpha polypeptide: Click to Expand ⟱
Source: CGL-Driver Genes
Type: Oncogene
PDGFRA (Platelet-Derived Growth Factor Receptor Alpha) is a receptor tyrosine kinase that plays a significant role in cell growth, survival, and differentiation. It is part of the PDGF family, which includes various growth factors that bind to PDGF receptors to regulate cellular functions.
Cancers, such as gastrointestinal stromal tumors (GISTs), are often associated with mutations in the PDGFRA gene.
Imatinib (Gleevec) is a tyrosine kinase inhibitor that is effective in treating GISTs with PDGFRA mutations.

PDGFRA overexpression is reported in several tumors. However, more notably, mutations (often gain-of-function) or gene amplifications in PDGFRA are key oncogenic events in certain cancer types.
Scientific Papers found: Click to Expand⟱
110- SFN,    Sulforaphane regulates self-renewal of pancreatic cancer stem cells through the modulation of Sonic hedgehog-GLI pathway
- in-vivo, PC, NA
HH↓, Hedgehog pathway blockade by SFN at a dose of 20 mg/kg resulted in a 45 % reduction in growth of pancreatic cancer tumors and reduced expression of Shh pathway components, Smo, Gli 1, and Gli 2 in mouse tissues.
Smo↓,
Gli1↓,
GLI2↓,
Shh↓,
VEGF↓, SFN inhibited the expression of pluripotency maintaining transcription factors Nanog and Oct-4 and angiogenic markers VEGF and PDGFRα which are downstream targets of Gli transcription
PDGFRA↓,
EMT↓, SFN treatment resulted in a significant reduction in EMT markers Zeb-1, which correlated with increase in E-Cadherin expression suggesting the blockade of signaling involved in early metastasis.
Zeb1↓,
Bcl-2↓, SFN downregulated the expression of Bcl-2 and XIAP to induce apoptosis.
XIAP↓,
E-cadherin↑,
OCT4↓,
Nanog↓,
TumCG↑, SFN results in marked reduction in EMT, metastatic, angiogenic markers with significant inhibition in tumor growth in mice.

1733- SFN,    Sonic Hedgehog Signaling Inhibition Provides Opportunities for Targeted Therapy by Sulforaphane in Regulating Pancreatic Cancer Stem Cell Self-Renewal
- in-vitro, PC, PanCSC - in-vitro, Nor, HPNE - in-vitro, Nor, HNPSC
CSCs↓, In an in vitro model, human pancreatic CSCs derived spheres were significantly inhibited on treatment with SFN
Shh↓, SFN inhibited the components of Shh pathway and Gli transcriptional activity
Gli↓,
Nanog↓, suppressing the expression of pluripotency maintaining factors (Nanog and Oct-4) as well as PDGFRα and Cyclin D1
OCT4↓,
PDGFRA↓,
cycD1/CCND1↑,
Apoptosis↑, SFN induced apoptosis by inhibition of BCL-2 and activation of caspases
Casp↑,
Smo↓, SFN inhibited the expression of Smo, Gli1 and Gli2.
Gli1↓,
GLI2↓,
Bcl-2↓, SFN induced apoptosis in pancreatic CSCs by inhibiting Bcl-2 expression and through the activation of caspase 3/7
Casp3↑,
Casp7↑,


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 ⓘ

XIAP↓, 1,  

Cell Death ⓘ

Apoptosis↑, 1,   Bcl-2↓, 2,   Casp↑, 1,   Casp3↑, 1,   Casp7↑, 1,  

Cell Cycle & Senescence ⓘ

cycD1/CCND1↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

CSCs↓, 1,   EMT↓, 1,   Gli↓, 1,   Gli1↓, 2,   HH↓, 1,   Nanog↓, 2,   OCT4↓, 2,   PDGFRA↓, 2,   Shh↓, 2,   Smo↓, 2,   TumCG↑, 1,  

Migration ⓘ

E-cadherin↑, 1,   GLI2↓, 2,   Zeb1↓, 1,  

Angiogenesis & Vasculature ⓘ

VEGF↓, 1,  
Total Targets: 22

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: PDGFRA, platelet-derived growth factor receptor, alpha polypeptide
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#:%  Target#:244  State#:%  Dir#:1
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