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首页> 外文期刊>Cellular Physiology and Biochemistry >XRCC2-Deficient Cells are Highly Sensitive to 5-Fluorouracil in Colorectal Cancer
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XRCC2-Deficient Cells are Highly Sensitive to 5-Fluorouracil in Colorectal Cancer

机译：XRCC2缺陷细胞对5-氟尿嘧啶在结直肠癌中高度敏感

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>Background/Aims: Inhibition of the repair of 5-fluorouracil (5-FU)-induced DNA lesions may improve the responses of tumors to anticancer agents. XRCC2 is a key factor in DNA repair. However, the role of XRCC2 in the chemoresistance of colorectal cancer (CRC) treated with 5-FU remains unclear. The aim of this study is to investigate whether XRCC2 expression affects the chemosensitivity of colorectal cancer. Methods: XRCC2 expression in CRC tissues was assessed, and the outcomes were analyzed to determine the clinical importance of XRCC2 expression. Following treatment with 5-FU, the effect of XRCC2 on proliferation was evaluated via a CCK-8 assay, the effects on cell cycle distribution and apoptosis were analyzed using flow cytometry, and ?3H2AX foci formation assays were performed to examine the influence of 5-FU on DNA Double-strand breaks(DSBs) repair in CRC cells. Results: XRCC2 expression in CRC tissues was significantly higher than that in normal tissues, and this increased XRCC2 expression was associated with advanced T staging, M staging, TNM staging, Dukea€?s staging, and greater liver and lymph node metastases. XRCC2 expression might be an independent prognostic indicator for CRC patients. Patients with negative XRCC2 expression exhibit greater sensitivity to treatment with 5-FU-based chemotherapy than those with positive XRCC2 expression. Moreover, our observations revealed that the knockdown of XRCC2 in CRC cells increased the sensitivities to 5-FU in terms of cell proliferation, apoptosis and cell cycle arrest. DNA DSBs repair was slower in the XRCC2-deficient cells than in the XRCC2-wild type cells. Conclusion: Our study demonstrated that XRCC2 might play an important role in CRC and function as a novel prognostic indicator and that the down-regulation of XRCC2 may be useful for sensitizing CRC cells during 5-FU chemotherapy.
机译：> 背景/目的： 抑制5-氟尿嘧啶（5-FU）诱导的DNA损伤的修复可能会改善肿瘤对抗癌药的反应。 XRCC2是DNA修复的关键因素。然而，XRCC2在用5-FU治疗的结直肠癌（CRC）的化学耐药性中的作用仍不清楚。这项研究的目的是调查XRCC2表达是否影响大肠癌的化学敏感性。 方法： 评估CRC组织中XRCC2的表达，并分析结局以确定XRCC2表达的临床重要性。用5-FU处理后，通过CCK-8分析评估XRCC2对增殖的影响，使用流式细胞术分析对XRCC2对细胞周期分布和凋亡的影响，并进行？3H2AX灶形成分析以检查5 -FU对CRC细胞中DNA双链断裂（DSBs）的修复作用。 结果： CRC组织中的XRCC2表达显着高于正常组织，并且这种XRCC2表达增加与晚期T分期，M分期，TNM分期，杜克大学有关。分期，以及更大的肝和淋巴结转移。 XRCC2表达可能是CRC患者的独立预后指标。 XRCC2表达阴性的患者比XRCC2表达阳性的患者对基于5-FU的化学疗法的治疗敏感性更高。此外，我们的观察结果表明，在细胞增殖，凋亡和细胞周期停滞方面，CRC细胞中XRCC2的敲低增加了对5-FU的敏感性。在XRCC2缺陷型细胞中，DNA DSB的修复要慢于在XRCC2野生型细胞中的修复。 结论： 我们的研究表明XRCC2可能在CRC中起重要作用，并作为一种新的预后指标，并且XRCC2的下调可能有助于致敏CRC细胞在5-FU化疗期间。

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