Radiosensitization by cyclin-dependent kinase inhibitors and its molecular mechanism

异硫氰酸酯（ITCs）具有肿瘤预防活性。ITCs诱导肿瘤抑制因子CKI （CDK抑制剂）如p21和p27的上调，并为正常细胞抗肿瘤提供保护作用。在这里，我们报道了萝卜硫素（SFN）和异硫氰酸苄酯（BITC）通过修复抑制辐射诱导的DNA双链断裂，通过损伤非同源末端连接（NHEJ）和同源重组修复（HRR）途径，增强人类肿瘤细胞的放射敏感性。SFN和BITC还协同增加辐射诱导的人肿瘤细胞凋亡。我们的数据表明SFN和BITC在不久的将来可能作为放射治疗的辅助手段。

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.