| Induction of p202, a modulator of apoptosis, during oncogenic transformation of NIH 3T3 cells by activated H-Ras (Q61L) contributes to cell survival. | |
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MedLine Citation:
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PMID: 12461788 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Previous studies have revealed that p202 (52 kDa), an interferon (IFN) and differentiation-inducible protein, negatively regulates cell proliferation and modulates cell survival. However, the role of p202 in transformed cells remains to be investigated. Here we report that constitutive expression of oncogenic H-Ras (Q61L) in NIH 3T3 cells, which resulted in cell transformation, was associated with increases in the steady-state levels of 202 RNA and protein. Interestingly, the increase in p202 levels in transformed cells correlated with increases in the activity of the transcription factor c-Jun/AP-1, which bound to the two potential AP-1 DNA binding sites (the AP-1CS1 and AP-1CS2) in the 5'-regulatory region of the 202 gene in gel mobility shift assays. Furthermore, the site-directed mutagenesis, coupled with promoter-reporter analyses, revealed that these two AP-1 DNA binding sites contribute to the regulation of the 202 gene in Ras transformed cells. Because treatment of transformed cells with a specific inhibitor of MEK (PD 98059) resulted in significant decreases in the levels of p202, these observations raise the possibility that in transformed cells Ras/Raf/MEK pathway regulates the transcriptional activation of the 202 gene. Significantly, decreases in the levels of p202 in Ras transformed NIH 3T3 cells under reduced serum conditions increased the susceptibility to apoptosis. Collectively, our observations support the idea that the transcriptional increases in the levels of p202 by oncogenic H-Ras in NIH 3T3 cells are needed for cell survival. |
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Authors:
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Hong Xin; Yanbiao Geng; Rocky Pramanik; Divaker Choubey |
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Publication Detail:
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Type: Journal Article; Research Support, U.S. Gov't, P.H.S. |
Journal Detail:
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Title: Journal of cellular biochemistry Volume: 88 ISSN: 0730-2312 ISO Abbreviation: J. Cell. Biochem. Publication Date: 2003 Jan |
Date Detail:
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Created Date: 2002-12-03 Completed Date: 2003-06-13 Revised Date: 2008-11-21 |
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: 191-204 Citation Subset: IM |
Copyright Information:
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Copyright 2002 Wiley-Liss, Inc. |
Affiliation:
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Department of Radiation Oncology, Stritch School of Medicine, Loyola University Medical Center, 2160 South First Avenue, Building No. 1, Mail code: 114B, Maywood, IL 60153, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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3T3 Cells Animals Apoptosis* Binding Sites Blotting, Northern Carrier Proteins / metabolism* Cell Survival Cell Transformation, Neoplastic* Cytoplasm / metabolism Flow Cytometry Genes, Reporter Genes, ras Genetic Vectors Immunoblotting Intracellular Signaling Peptides and Proteins* Mice Mutagenesis, Site-Directed Phosphoproteins / metabolism* Plasmids / metabolism Promoter Regions, Genetic Proto-Oncogene Proteins p21(ras) / metabolism Reverse Transcriptase Polymerase Chain Reaction Time Factors Transfection |
| Grant Support | |
ID/Acronym/Agency:
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CA69031/CA/NCI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Carrier Proteins; 0/Ifi202b protein, mouse; 0/Intracellular Signaling Peptides and Proteins; 0/Phosphoproteins; EC 3.6.5.2/Proto-Oncogene Proteins p21(ras) |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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