期刊
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
卷 377, 期 2, 页码 341-345出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2008.09.150
关键词
Sulforaphane (SFN); DNA double strand breaks (DSBs); Homologous recombination repair (HRR); Non-homologous end joining (NHEJ)
资金
- Japan Society for the Promotion of Science (JSPS) [16209036]
- Grants-in-Aid for Scientific Research [16209036] Funding Source: KAKEN
Cytotoxicity and DNA double strand breaks (DSBs) were studied in HeLa cells treated With Sulforaphane (SFN), a well-known chemo-preventive agent. Cell survival was impaired by SFN in a concentration and treatment time-dependent manner. Both constant field gel electrophoresis (CFGE) and gamma-H2AX assay unambiguously indicated formation of DSBs by SFN, reflecting the cell Survival data. These DSBs were predominantly processed by homologous recombination repair (HRR), judging from the SFN concentration-dependent manner of Rad51 foci formation. On the other hand, the phosphorylation of DNA-PKcs, a key non-homologous end joining (NHEJ) protein, was not observed by SFN treatment, suggesting that NHEJ may not be involved in DSBs induced by this chemical. G2/M arrest by SFN, a typical response for cells exposed to ionizing radiation was also observed. Our new data indicate the clear induction of DSBs by SFN and a useful anti-tumour aspect of SFN through the induction of DNA DSBs. (C) 2008 Elsevier Inc. All rights reserved.
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