Radiosensitization by cyclin-dependent kinase inhibitors and its molecular mechanism

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Isothiocyanates (ITCs) exhibit tumor prevention acivity. ITCs induce the upregulation of tumor suppressors CKI (CDK inhibitor) such as p21 and p27, and provide a protective effect to normal cells against cancer. Here, we report that Sulforaphane (SFN) and Benzyl isothiocyanate (BITC), enhance radiosensitivity in human tumor cells by repair inhibition of radiation-induced DNA double strand breaks through the impairment of nonhomologous end joining (NHEJ) and homologous recombination repair (HRR) pathways. SFN and BITC also synergisitically increase the radiation-induced apoptosis in human tumor cells. Our data suggest the potential use of SFN and BITC as an adjuvant to radiation therapy in the near future.