Document Detail

Multiple regulatory pathways of vascular permeability factor/vascular endothelial growth factor (VPF/VEGF) expression in tumors.
MedLine Citation:
PMID:  15018896     Owner:  NLM     Status:  MEDLINE    
VPF/VEGF is a multi-functional cytokine with important roles in both vasculogenesis and angiogenesis. Its production is generally regulated by local oxygen concentration. Hypoxia stimulates VPF/VEGF production by increasing its gene transcription and the stability of its mRNA. The increase in transcription in hypoxia occurs mainly through the stabilization and activation of the transcription factor, Hypoxia Inducible Factor (HIF). Cellular oxygen concentration is not the only regulator of VPF/VEGF synthesis. Some cancer cells can produce high levels of VPF/VEGF even in normoxia. Clear cell renal carcinoma cell line (RCC) like 786-0, pancreatic carcinoma cell line, ASPC-1, fibrocarcinoma cell line, HT1080, ovarian cancer cells, etc. produce an elevated level of VPF/VEGF, which is not dependent on hypoxia. In this article, we discuss different regulatory pathways in tumor cells comprised of oncogenes, tumor suppressor genes etc. that play important roles, in both the transcription and stability of VPF/VEGF mRNA.
Debabrata Mukhopadhyay; Kaustubh Datta
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review    
Journal Detail:
Title:  Seminars in cancer biology     Volume:  14     ISSN:  1044-579X     ISO Abbreviation:  Semin. Cancer Biol.     Publication Date:  2004 Apr 
Date Detail:
Created Date:  2004-03-15     Completed Date:  2004-10-12     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  9010218     Medline TA:  Semin Cancer Biol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  123-30     Citation Subset:  IM    
Department of Pathology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA 02215, USA.
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MeSH Terms
Basic Helix-Loop-Helix Transcription Factors
DNA-Binding Proteins / metabolism
Gene Expression Regulation, Neoplastic*
Genes, Tumor Suppressor
Hypoxia-Inducible Factor 1
Hypoxia-Inducible Factor 1, alpha Subunit
Neoplasms / blood supply,  genetics*,  metabolism
Neovascularization, Pathologic / metabolism
Nuclear Proteins / metabolism
Oncogenes / genetics
Protein Kinase C / metabolism
Proteins / metabolism
RNA Stability / genetics
Signal Transduction
Transcription Factors*
Tumor Suppressor Protein p53 / metabolism
Tumor Suppressor Proteins / metabolism
Ubiquitin-Protein Ligases / metabolism
Up-Regulation / genetics
Vascular Endothelial Growth Factor A / biosynthesis,  genetics*
Von Hippel-Lindau Tumor Suppressor Protein
src-Family Kinases / metabolism
Grant Support
Reg. No./Substance:
0/Basic Helix-Loop-Helix Transcription Factors; 0/DNA-Binding Proteins; 0/HIF1A protein, human; 0/Hypoxia-Inducible Factor 1; 0/Hypoxia-Inducible Factor 1, alpha Subunit; 0/Nuclear Proteins; 0/Proteins; 0/Transcription Factors; 0/Tumor Suppressor Protein p53; 0/Tumor Suppressor Proteins; 0/Vascular Endothelial Growth Factor A; 0/endothelial PAS domain-containing protein 1; EC Kinases; EC Kinase C; EC Ligases; EC protein, human; EC Hippel-Lindau Tumor Suppressor Protein

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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