Abstract: AIM: To investigate the mechanisms un-derlying the antitumoreffect of trichostatin A(TSA)on LNCaPprostate cancercell line.METHODS: Prolifera-tion of LNCaPcells exposed to TSA was detected by MTT assay.Cell apoptosis was assayed by Hoechst 33342 nu-clei staining.Western blotting was performed to analyze the expression of the androgen receptor(AR)afterTSA exposure.Semi-quantitative RT-PCrwas used to assay the transcription changes of AR.RESULTS: TSA kills LNCaPcellswith an ED 50 value of 125.9 nmol·L-1 with-in 48 hours exposure.TSA inhibited LNCaPcell prolifer-ation aswell as inducing cell apoptosis.TSA depleted Arboth in a dose and time dependent manner.Moreover,the expression of cell cycle-dependent kinase inhibitor,p21,was induced.The decreasing of Aroccurred at the protein level instead of transcription suppression.CONCLUSION: TSA exhibits significant antitumoreffect against LNCaPcells through depletion of AR.

Key words: prostatic neoplasms, receptors,andro-gen, apoptosis, histone deacetylases, histone deacetylase inhibitors, trichostatin A, cell signaling pathway