The histone deacetylase inhibitor, Trichostatin A, induces G2/M phase arrest and apoptosis in YD-10B oral squamous carcinoma cells

Histone acetylation is one of the key chromatin modifications that controlgene transcription during development and tumorigenesis. Recently, it was reportedthat the histone deacetylase inhibitor, Trichostatin A (TSA), induces growth arrestand apoptosis in tumors. However, the molecular mechanisms responsible for itsantitumor effects are not clear. The purpose of this study was to investigatethe effect of TSA on human oral squamous carcinoma cells and to determine themechanisms underlying the antitumor activity of TSA. MTT assays showed that TSAinhibited cell proliferation in YD-10B cells. TSA also effectively arrested cellcycle progression at the G2/M phase through the up-regulation of p21waf expression,down-regulation of Cyclin B1 and reduction of the inhibitory phophorylation ofCdc2. In addition, mitochondrial membrane destruction was induced by a 48 h TSAtreatment. TSA also induced cytochrome c release and proteolytic activation ofcaspase 3 and caspase 7 in YD-10B cells. Taken together, these observations inYD-10B oral cancer cells reveal the potential value of TSA in inhibiting oraltumor growth.