Abstract Title:

Sulforaphane induces DNA double strand breaks predominantly repaired by homologous recombination pathway in human cancer cells.

Abstract Source:

Biochem Biophys Res Commun. 2008 Dec 12;377(2):341-5. Epub 2008 Oct 12. PMID: 18854174

Abstract Author(s):

Emiko Sekine-Suzuki, Dong Yu, Nobuo Kubota, Ryuichi Okayasu, Kazunori Anzai

Article Affiliation:

Heavy-Ion Radiobiology Research Group, Research Center for Charged Particle Therapy, National Institute of Radiological Sciences, 4-9-1 Anagawa, Inage-ku, Chiba 263-8555, Japan.

Abstract:

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-tumor aspect of SFN through the induction of DNA DSBs.

Study Type : In Vitro Study

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