Document Detail


Transcription factor TFII-I causes transcriptional upregulation of GRP78 synthesis in prostate cancer cells.
MedLine Citation:
PMID:  19097122     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Receptor-recognized forms of alpha(2)-macroglobulin (alpha(2)M*) bind to cell surface-associated GRP78 and induce proliferative and survival signaling in prostate cancer cells. As part of the cellular response to alpha(2)M*, GRP78 expression is itself upregulated. In response to other stimuli, the transcription factor TFII-I upregulates GRP78 by binding to its gene promoter. We have, therefore, studied the role of TFII-I in transcriptional upregulation of GRP78 in 1-LN human prostate cancer cells stimulated with alpha(2)M*. This treatment caused a two- to threefold increase in TFII-I and GRP78 synthesis from [(35)S]-labeled precursor amino acids. Synthesis of both TFII-I and GRP78 were significantly reduced by silencing TFII-I gene expression or pretreatment of cells with genistein or actinomycin D. Confocal microscopy was employed to demonstrate relocation of TFII-I to the nucleus. In alpha(2)M*-stimulated cells, moreover, TFII-I bound to the GRP78 promoter as determined by CHIP assay. We also demonstrate binding of TFII-I to the c-fos promoter, consistent with its role in upregulating c-fos gene expression. In non-lymphoid cells, phosphorylated c-Src is an activator of TFII-I. Ligation of GRP78 on 1-LN cells with alpha(2)M* was followed by tyrosine phosphorylation of c-Src as well as TFII-I. We conclude that alpha(2)M*-induced increase in GRP78 synthesis is caused by transcriptional upregulation of TFII-I which binds to the GRP78 promoter and thus potentiates its cell survival and antipoptotic functions in 1-LN prostate cancer cells.
Authors:
U K Misra; F Wang; S V Pizzo
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural    
Journal Detail:
Title:  Journal of cellular biochemistry     Volume:  106     ISSN:  1097-4644     ISO Abbreviation:  J. Cell. Biochem.     Publication Date:  2009 Feb 
Date Detail:
Created Date:  2009-01-27     Completed Date:  2009-03-23     Revised Date:  2011-11-02    
Medline Journal Info:
Nlm Unique ID:  8205768     Medline TA:  J Cell Biochem     Country:  United States    
Other Details:
Languages:  eng     Pagination:  381-9     Citation Subset:  IM    
Affiliation:
Department of Pathology, Duke University Medical Center, Durham, North Carolina 27710, USA.
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MeSH Terms
Descriptor/Qualifier:
Cell Line, Tumor
Gene Expression Regulation, Neoplastic / drug effects,  genetics*
Heat-Shock Proteins / biosynthesis,  genetics*
Humans
Male
Molecular Chaperones / biosynthesis,  genetics*
Phosphorylation
Phosphotyrosine / metabolism
Prostatic Neoplasms / genetics*,  metabolism,  pathology*
Protein Binding
Protein Transport
Protein-Tyrosine Kinases / metabolism
Proto-Oncogene Proteins / metabolism
Proto-Oncogene Proteins c-fos / metabolism
RNA Interference
Transcription Factors, TFII / genetics,  metabolism*
Transcription, Genetic / drug effects,  genetics*
Up-Regulation / drug effects,  genetics*
alpha-Macroglobulins / pharmacology
Grant Support
ID/Acronym/Agency:
HL-24066/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/GTF2I protein, human; 0/Heat-Shock Proteins; 0/Molecular Chaperones; 0/Proto-Oncogene Proteins; 0/Proto-Oncogene Proteins c-fos; 0/Transcription Factors, TFII; 0/alpha-Macroglobulins; 0/molecular chaperone GRP78; 21820-51-9/Phosphotyrosine; EC 2.7.10.1/Protein-Tyrosine Kinases; EC 2.7.10.2/CSK tyrosine-protein kinase

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


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