Role for CITED2, a CBP/p300 interacting protein, in colon cancer cell invasion

被引:47
作者
Bai, Longchuan [1 ]
Merchant, Juanita L. [1 ,2 ]
机构
[1] Univ Michigan, Dept Internal Med, Ann Arbor, MI 48109 USA
[2] Univ Michigan, Dept Mol & Integrat Physiol, Ann Arbor, MI 48109 USA
关键词
histone deacetylase inhibitor; butyrate; matrix metalloproteinase-13; beta-catenin;
D O I
10.1016/j.febslet.2007.11.072
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
A thorough understanding of histone acetyltransferase CBP/p300-mediated regulation of gene expression and cell growth is essential to identify mechanisms relevant to the development of histone deacetylase (HDAC) inhibitor-based preventive and therapeutic strategies. We found that knockdown of CBP/p300 interacting coactivator with glutamic acid/aspartic acid-rich tail 2 (CITED2) increased colon cancer cell invasiveness in vitro. Gene expression pro. ling revealed that CITED2 knockdown induced matrix metalloproteinase-13 (MMP-13) gene expression in colon cancer cells. Butyrate, a naturally occurring HDAC inhibitor, induced CITED2 expression and downregulated MMP-13 expression in RKO cells. Additionally, ectopic expression of CITED2 arrested RKO cell growth. Thus, CITED2 regulates colon cancer invasion and might be a target for HDAC inhibitor-based intervention of colon cancer. (c) 2007 Federation of European Biochemical Societies. Published by Elsevier B. V. All rights reserved.
引用
收藏
页码:5904 / 5910
页数:7
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