Literature DB >> 16751067

Histone deacetylase inhibitors enhance phosphorylation of histone H2AX after ionizing radiation.

Yubin Zhang1, Masaaki Adachi, Huichao Zou, Masato Hareyama, Kohzoh Imai, Yasuhisa Shinomura.   

Abstract

PURPOSE: Histone deacetylase (HDAC) inhibitors are believed to be promising radiosensitizers. To explore their effects on ionizing radiation (IR), we examined whether the HDAC inhibitors m-carboxycinnamic acid bis-hydroxamide (CBHA) and depsipeptide FK228 affect H2AX phosphorylation (gamma-H2AX), a landmark of DNA double-strand breaks after IR exposure. METHODS AND MATERIALS: We evaluated the effects of the HDAC inhibitors on clonogenic assay in human lung carcinoma A549 cells and progression of A549 xenograft tumors. IR-induced DNA damage was evaluated by histone gamma-H2AX. Histone hyperacetylation was induced by overexpression of histone acetyltransferase p300 and evaluated by Western blots.
RESULTS: M-carboxycinnamic acid bishydroxyamide pretreatment radiosensitized A549 cells and strongly inhibited A549 xenograft tumor progression. CBHA and FK228, but not 5-fluorouracil, enhanced IR-induced gamma-H2AX in A549 and other cancer cell lines. Overexpression of p300 similarly augmented IR-induced gamma-H2AX.
CONCLUSION: The results of this study suggest that HDAC inhibitors enhance IR-induced gamma-H2AX, most likely through histone hyperacetylation, and radiosensitize various cancers.

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Year:  2006        PMID: 16751067     DOI: 10.1016/j.ijrobp.2006.03.019

Source DB:  PubMed          Journal:  Int J Radiat Oncol Biol Phys        ISSN: 0360-3016            Impact factor:   7.038


  12 in total

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