| Transcription factor TFII-I causes transcriptional upregulation of GRP78 synthesis in prostate cancer cells. | |
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MedLine Citation:
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PMID: 19097122 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
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Authors:
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U K Misra; F Wang; S V Pizzo |
Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural |
Journal Detail:
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Title: Journal of cellular biochemistry Volume: 106 ISSN: 1097-4644 ISO Abbreviation: J. Cell. Biochem. Publication Date: 2009 Feb |
Date Detail:
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Created Date: 2009-01-27 Completed Date: 2009-03-23 Revised Date: 2011-11-02 |
Medline Journal Info:
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Nlm Unique ID: 8205768 Medline TA: J Cell Biochem Country: United States |
Other Details:
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Languages: eng Pagination: 381-9 Citation Subset: IM |
Affiliation:
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Department of Pathology, Duke University Medical Center, Durham, North Carolina 27710, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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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:
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HL-24066/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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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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