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| Research article summary (published 20 Jan 2007): |
The RNA-binding protein Sam68 contributes to proliferation and survival of human prostate cancer cells.
Full Abstract
The tyrosine kinase Src is frequently activated in advanced human prostate carcinomas and its activation correlates with tyrosine phosphorylation of the RNA-binding protein Sam68. Herein, we have investigated the expression and function of Sam68 in human prostate cancer cells. Analysis of specimens obtained from 20 patients revealed that Sam68 is upregulated at the protein level in 35% of the samples. Real-time polymerase chain reaction confirmed the results at the mRNA level in most patients. Downregulation of Sam68 by RNAi in LNCaP prostate cancer cells delayed cell cycle progression and reduced the proliferation rate. Moreover, depletion of Sam68 sensitized cells to apoptosis induced by DNA-damaging agents. Similarly, stable cell lines expressing a truncated GFP-Sam68(GSG) protein displayed reduced growth rates and higher sensitivity to cisplatin-induced apoptosis. Microarray analyses revealed that a subset of genes involved in proliferation and apoptosis were altered when Sam68 was knocked down in LNCaP cells. Our results indicate that Sam68 expression supports prostate cancer cells proliferation and survival to cytotoxic agents.
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Author information
Author/s: Busą, R (R); Paronetto, M P (MP); Farini, D (D); Pierantozzi, E (E); Botti, F (F); Angelini, D F (DF); Attisani, F (F); Vespasiani, G (G); Sette, C (C);
Affiliation: Department of Public Health and Cell Biology, University of Rome Tor Vergata, Rome, Italy.
Journal and publication information
Publication Type: Journal Article; Research Support, Non-U.S. Gov't
Journal: Oncogene (Oncogene), published in England. (Language: eng)
Reference: 2007-Jun; vol 26 (issue 30) : pp 4372-82
Dates: Created 2007/06/28; Completed 2007/08/02;
PMID: 17237817, status: MEDLINE (last retrieval date: 12/26/2008)
Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.
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