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同源重组作为哺乳动物细胞中咖啡因放射增敏的潜在靶点:XRCC2和XRCC3突变体中咖啡因放射增敏作用降低

Homologous recombination as a potential target for caffeine radiosensitization in mammalian cells: reduced caffeine radiosensitization in XRCC2 and XRCC3 mutants.

作者信息

Asaad N A, Zeng Z C, Guan J, Thacker J, Iliakis G

机构信息

Department of Radiation Oncology of Kimmel Cancer Center, Jefferson Medical College, Philadelphia, Pennsylvania 19107, USA.

出版信息

Oncogene. 2000 Nov 23;19(50):5788-800. doi: 10.1038/sj.onc.1203953.

Abstract

The radiosensitizing effect of caffeine has been associated with the disruption of multiple DNA damage-responsive cell cycle checkpoints, but several lines of evidence also implicate inhibition of DNA repair. The role of DNA repair inhibition in caffeine radiosensitization remains uncharacterized, and it is unknown which repair process, or lesion, is affected. We show that a radiosensitive cell line, mutant for the RAD51 homolog XRCC2 and defective in homologous recombination repair (HRR), displays significantly diminished caffeine radiosensitization that can be restored by expression of XRCC2. Despite the reduced radiosensitization, caffeine effectively abrogates checkpoints in S and G2 phases in XRCC2 mutant cells indicating that checkpoint abrogation is not sufficient for radiosensitization. Another radiosensitive line, mutant for XRCC3 and defective in HRR, similarly shows reduced caffeine radiosensitization. On the other hand, a radiosensitive mutant (irs-20) of DNA-PKcs with a defect in non-homologous end-joining (NHEJ) is radiosensitized by caffeine to an extent comparable to wild-type cells. In addition, rejoining of radiation-induced DNA DSBs, that mainly reflects NHEJ, remains unaffected by caffeine in XRCC2 and XRCC3 mutants, or their wild-type counterparts. These observations suggest that caffeine targets steps in HRR but not in NHEJ and that abrogation of checkpoint response is not sufficient to explain radiosensitization. Indeed, immortalized fibroblasts from AT patients show caffeine radiosensitization despite the checkpoint defects associated with ATM mutation. We propose that caffeine radiosensitization is mediated by inhibition of stages in DNA DSB repair requiring HRR and that checkpoint disruption contributes by allowing these DSBs to transit into irreparable states. Thus, checkpoints may contribute to genomic stability by promoting error-free HRR.

摘要

咖啡因的放射增敏作用与多个DNA损伤反应性细胞周期检查点的破坏有关,但也有几条证据表明其对DNA修复有抑制作用。DNA修复抑制在咖啡因放射增敏中的作用仍未明确,且不清楚哪个修复过程或损伤受到影响。我们发现,一种对辐射敏感的细胞系,其RAD51同源物XRCC2发生突变且同源重组修复(HRR)存在缺陷,该细胞系对咖啡因的放射增敏作用显著减弱,而XRCC2的表达可恢复这种作用。尽管放射增敏作用降低,但咖啡因能有效消除XRCC2突变细胞中S期和G2期的检查点,这表明检查点的消除不足以实现放射增敏。另一种对辐射敏感的细胞系,其XRCC3发生突变且HRR存在缺陷,同样显示出对咖啡因的放射增敏作用降低。另一方面,DNA-PKcs的一个对辐射敏感的突变体(irs-20),其非同源末端连接(NHEJ)存在缺陷,对咖啡因的放射增敏程度与野生型细胞相当。此外,辐射诱导的DNA双链断裂(DSB)的重新连接主要反映NHEJ,在XRCC2和XRCC3突变体及其野生型对应物中,咖啡因对其均无影响。这些观察结果表明,咖啡因作用于HRR中的步骤而非NHEJ中的步骤,且检查点反应的消除不足以解释放射增敏作用。事实上,来自共济失调毛细血管扩张症(AT)患者的永生化成纤维细胞尽管存在与ATM突变相关的检查点缺陷,但仍显示出对咖啡因的放射增敏作用。我们提出,咖啡因的放射增敏作用是由抑制DNA DSB修复中需要HRR的阶段介导的,而检查点的破坏则通过使这些DSB转变为无法修复的状态来发挥作用。因此,检查点可能通过促进无差错的HRR来维持基因组稳定性。

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