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A role for CITED2, a CBP/p300 interacting protein, in colon cancer cell invasion
Author(s) -
Bai Longchuan,
Merchant Juanita L.
Publication year - 2007
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2007.11.072
Subject(s) - gene knockdown , cancer research , coactivator , histone deacetylase , ectopic expression , histone deacetylase inhibitor , biology , histone acetyltransferase , butyrate , cell growth , gene expression , chemistry , microbiology and biotechnology , histone , cell culture , gene , biochemistry , transcription factor , genetics , fermentation
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 profiling 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.