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Cancer Res Treat. 2005 Apr;37(2):122-128. English. Original Article.
Kim IA , Kim JH , Shin JH , Kim IH , Kim JS , Wu HG , Chie EK , Kim YH , Kim BK , Hong S , Park SW , Ha SW , Park CI .
Department of Radiation Oncology, Seoul National University College of Medicine, Seoul, Korea. ihkim@snu.ac.kr
Cancer Research Institute, Seoul National University College of Medicine, Seoul, Korea.
Institute of Radiation Medicine, Seoul National University College of Medicine, Seoul, Korea.
Department of Radiation Oncology, Seoul National University Bundang Hospital, Seongnam, Korea.
Department of Radiation Oncology, Soonchunhyang University College of Medicine, Bucheon, Korea.
Department of Radiation Oncology, Dankook University College of Medicine, Cheonan, Korea.
Department of Radiation Oncology, Konkuk University College of Medicine, Seoul, Korea.
Department of Radiation Oncology, Chung-Ang University College of Medicine, Seoul, Korea.
Abstract

PURPOSE: Histone deacetylase inhibitors (HDIs) are emerging as potentially useful components in anticancer therapy. In this study, we tried to confirm the radiosensitizing effect of trichostatin A (TSA) on a panel of human carcinoma cell lines and elucidate its mechanism of interaction. MATERIALS AND METHODS: A549, HeLa and Caski cells were exposed to TSA for 18 hr prior to irradiation, and the cell survival then measured using a clonogenic assay. Western blot and flow cytometric analyses, for histone acetylation, and cell cycle and apoptosis, respectively, were also performed. RESULTS: TSA increased the acetylation of histone H3. The pretreatment of TSA consistently radiosensitized all three cell lines. The SF2 (surviving fraction at 2 Gy) of TSA-treated cells was significantly lower than that of mock treated cells. The SER (sensitizer enhancement ratio) increased in all 3 cell lines, in concentration dependent manners. The TSA treated cells showed abrogation of radiation-induced G2/M arrest, in a concentration dependent manner. CONCLUSION: The pretreatment of TSA enhanced the radiosensitivity of a panel of human carcinoma cells, which was attributed, in part, to the abrogation of radiationinduced G2/M arrest.

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