Document Detail


HEXIM1 modulates vascular endothelial growth factor expression and function in breast epithelial cells and mammary gland.
MedLine Citation:
PMID:  20453883     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Recently, we found that mutation of the C-terminus of transcription factor hexamethylene bisacetamide-inducible protein 1 (HEXIM1) in mice leads to abnormalities in cardiovascular development because of aberrant vascular endothelial growth factor (VEGF) expression. HEXIM1 regulation of some genes has also been shown to be positive transcription elongation factor b (P-TEFb) dependent. However, it is not known whether HEXIM1 regulates VEGF in the mammary gland. We demonstrate that HEXIM1 regulates estrogen-induced VEGF transcription through inhibition of estrogen receptor-alpha recruitment to the VEGF promoter in a P-TEFb-independent manner in MCF-7 cells. Under hypoxic conditions, HEXIM1 inhibits estrogen-induced hypoxia-inducible factor-1 alpha (HIF-1alpha) protein expression and recruitment of HIF-1alpha to the hypoxia-response element in the VEGF promoter. In the mouse mammary gland, increased HEXIM1 expression decreased estrogen-driven VEGF and HIF-1alpha expression. Conversely, a mutation in the C-terminus of HEXIM1 (HEXIM1(1-312)) led to increased VEGF and HIF-1alpha expression and vascularization in mammary glands of heterozygous HEXIM1(1-312) mice when compared with their wild-type littermates. In addition, HEXIM1(1-312) mice have a higher incidence of carcinogen-induced mammary tumors with increased vascularization, suggesting an inhibitory role for HEXIM1 during angiogenesis. Taken together, our data provide evidence to suggest a novel role for HEXIM1 in cancer progression.
Authors:
N Ogba; Y Q Doughman; L J Chaplin; Y Hu; M Gargesha; M Watanabe; M M Montano
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.     Date:  2010-05-10
Journal Detail:
Title:  Oncogene     Volume:  29     ISSN:  1476-5594     ISO Abbreviation:  Oncogene     Publication Date:  2010 Jun 
Date Detail:
Created Date:  2010-06-24     Completed Date:  2010-07-16     Revised Date:  2011-12-22    
Medline Journal Info:
Nlm Unique ID:  8711562     Medline TA:  Oncogene     Country:  England    
Other Details:
Languages:  eng     Pagination:  3639-49     Citation Subset:  IM    
Affiliation:
Department of Pharmacology, Rainbow Babies and Children's Hospital, Cleveland, OH, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Carcinogens / toxicity
Cell Hypoxia / drug effects
Cell Line, Tumor
Epithelial Cells / drug effects,  metabolism*,  pathology
Estradiol / pharmacology
Estrogen Receptor alpha / metabolism
Gene Expression Regulation*
Humans
Hypoxia-Inducible Factor 1, alpha Subunit / metabolism
Mammary Glands, Animal / blood supply,  drug effects,  metabolism*,  pathology
Mammary Neoplasms, Experimental / chemically induced,  metabolism,  pathology,  physiopathology
Mice
Mutation
Neovascularization, Pathologic / metabolism
Neovascularization, Physiologic
Positive Transcriptional Elongation Factor B / metabolism
Promoter Regions, Genetic / genetics
RNA-Binding Proteins / chemistry,  genetics,  metabolism*
Response Elements
Vascular Endothelial Growth Factor A / genetics*,  metabolism*
Grant Support
ID/Acronym/Agency:
CA92440/CA/NCI NIH HHS; R01 CA092440-07/CA/NCI NIH HHS; R01 CA092440-10/CA/NCI NIH HHS
Chemical
Reg. No./Substance:
0/Carcinogens; 0/Estrogen Receptor alpha; 0/HEXIM1 protein, human; 0/Hif1a protein, mouse; 0/Hypoxia-Inducible Factor 1, alpha Subunit; 0/RNA-Binding Proteins; 0/Vascular Endothelial Growth Factor A; 50-28-2/Estradiol; EC 2.7.11.-/Positive Transcriptional Elongation Factor B

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


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