HDAC2, a class I HDAC, is significantly upregulated during early stages of tumor development and the increase becomes more profound as lesions progress from adenoma to adenocarcinoma in colorectal carcinogenesis. In vitro studies demonstrate that HDAC2 expression and activity are required to maintain a transformed phenotype with resistance to apoptosis in cultured HT-29 colonic cancer cells. This evidence clearly demonstrates that elevated HDAC2 expression contributes to colon cancer progression in an APC/b-catenin/TCF–dependent pathway mechanism. On the basis of its association with colon cancer progression, HDAC2 has been considered a potential target for colon cancer prevention and treatment.
Ravillah D, Mohammed A, Qian L, et al. Chemopreventive effects of an HDAC2-selective inhibitor on rat colon carcinogenesis and APCmin/+ mouse intestinal tumorigenesis[J]. Journal of Pharmacology and Experimental Therapeutics, 2014, 348(1): 59-68.