| Literature DB >> 19883641 |
Sonia I Vlaicu1, Cosmin A Tegla, Cornelia D Cudrici, Matthew Fosbrink, Vingh Nguyen, Philippe Azimzadeh, Violeta Rus, Hegang Chen, Petru A Mircea, Abulkalam Shamsuddin, Horea Rus.
Abstract
First described as a cell cycle activator, RGC-32 is both an activator and a substrate for CDC2. Deregulation of RGC-32 expression has been detected in a wide variety of human cancers. We have now shown that RGC-32 is expressed in precancerous states, and its expression is significantly higher in adenomas than in normal colon tissue. The expression of RGC-32 was higher in advanced stages of colon cancer than in precancerous states or the initial stages of colon cancer. In order to identify the genes that are regulated by RGC-32, we used gene array analysis to investigate the effect of RGC-32 knockdown on gene expression in the SW480 colon cancer cell line. Of the 230 genes that were differentially regulated after RGC-32 knockdown, a group of genes involved in chromatin assembly were the most significantly regulated in these cells: RGC-32 knockdown induced an increase in acetylation of histones H2B lysine 5 (H2BK5), H2BK15, H3K9, H3K18, and H4K8. RGC-32 silencing was also associated with decreased expression of SIRT1 and decreased trimethylation of histone H3K27 (H3K27me3). In addition, RGC-32 knockdown caused a significantly higher percentage of SW480 cells to enter S phase and subsequently G2/M. These data suggest that RGC-32 may contribute to the development of colon cancer by regulating chromatin assembly. Copyright 2009 Elsevier Inc. All rights reserved.Entities:
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Year: 2009 PMID： 19883641 PMCID： PMC2815209 DOI： 10.1016/j.yexmp.2009.10.010
Source DB: PubMed Journal: Exp Mol Pathol ISSN： 0014-4800 Impact factor: 3.362