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首页> 外文期刊>Cancer letters >Deleted in breast cancer 1 (DBC1) deficiency results in apoptosis of breast cancer cells through impaired responses to UV-induced DNA damage
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Deleted in breast cancer 1 (DBC1) deficiency results in apoptosis of breast cancer cells through impaired responses to UV-induced DNA damage

机译：在乳腺癌1（DBC1）缺乏症中缺失会导致对紫外线诱导的DNA损伤的反应减弱而导致乳腺癌细胞凋亡

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摘要

DBC1 (deleted in breast cancer 1) participates in the regulation of cell survival and death in response to various stimuli. In particular, DBC1 promotes cell death upon DNA damage through inhibition of SIRT1 deacetylase. However, the SIRT1-independent functions of DBC1 in the regulation of DNA damage response are less well understood. Therefore, we analyzed the DNA damage response in Hs578T breast cancer cell line in which the DBC1-SIRT1 interaction is barely detectable. DBC1-siRNA transfected cells showed a failure in the DNA damage checkpoint and the accumulation of genomic damage following UV irradiation. In addition, DBC1-deficient cells exhibited less JNK activation. Finally, the interruptions of signaling in DBC1-depleted cells contributed to cell death in response to UV irradiation. Overall, these data suggest that DBC1 is essential for a fully efficient and effective response to UV irradiation. Therefore, DBC1 plays a critical role in maintaining genomic stability and cellular integrity following UV-induced genotoxic stress.
机译：DBC1（在乳腺癌1中已删除）响应各种刺激参与细胞存活和死亡的调节。特别是，DBC1通过抑制SIRT1脱乙酰基酶促进DNA损伤时的细胞死亡。但是，DBC1在调节DNA损伤反应中不依赖SIRT1的功能还不太清楚。因此，我们分析了Hs578T乳腺癌细胞系中几乎检测不到DBC1-SIRT1相互作用的DNA损伤反应。 DBC1-siRNA转染的细胞在DNA损伤检查点显示失败，并在紫外线照射后出现基因组损伤积累。此外，DBC1缺陷细胞表现出较少的JNK激活。最后，在消耗DBC1的细胞中信号传递的中断导致了细胞对紫外线照射的死亡。总体而言，这些数据表明DBC1对于完全有效地响应UV辐射至关重要。因此，DBC1在紫外线诱导的遗传毒性胁迫后，在维持基因组稳定性和细胞完整性方面起着至关重要的作用。

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