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Effects of gamma irradiation on cell cycle apoptosis and telomerase activity in p53 wild-type and deficient HCT116 colon cancer cell lines

机译:γ射线对p53野生型和缺陷HCT116结肠癌细胞系细胞周期凋亡和端粒酶活性的影响

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摘要

Radiotherapy serves as adjunctive treatment to chemotherapy and surgical resection of colorectal cancer. However, the cellular response to irradiation varies depending on the expression of tumor suppressor p53, which plays a significant role in the regulation of cell cycle arrest, apoptosis and telomerase activity in various cancers. The present study aimed to investigate cell cycle arrest, apoptosis and telomerase activity with respect to p53 expression in p53 wild-type (+/+) and deficient (−/−) HCT116 colon cancer cell lines following 5 Gy γ-irradiation. Cell cycle arrest and apoptosis were evaluated using flow cytometry. The telomerase activity was measured using a TRAP (telomerase repeat amplification protocol) assay. Following treatment with irradiation, G1/S cell cycle arrest occurred in the p53+/+ cells, whereas the p53−/− cells accumulated in the G2 phase. No differences were observed in the apoptotic ratios between the two cell lines following irradiation. Decreased telomerase activity was observed in the p53+/+ cells, whereas telomerase activity was increased in the p53−/− cells. The results showed that while telomerase activity and G1 cell cycle arrest were regulated depending on the p53 status, G2 arrest and the apoptotic response were promoted via a p53-independent pathway.
机译:放射疗法可作为结直肠癌化学疗法和手术切除的辅助治疗。但是,细胞对辐射的反应取决于肿瘤抑制物p53的表达,而p53的表达在各种癌症的细胞周期停滞,凋亡和端粒酶活性的调节中起着重要作用。本研究旨在研究5 Gyγ射线照射后p53野生型(+ / +)和缺陷(-/-)HCT116结肠癌细胞系中p53表达的细胞周期阻滞,凋亡和端粒酶活性。使用流式细胞仪评估细胞周期停滞和凋亡。使用TRAP(端粒酶重复扩增方案)测定法测量端粒酶活性。放射线处理后,p53 + / +细胞发生了G1 / S细胞周期停滞,而p53-/-细胞则在G2期积累。照射后,两个细胞系之间的凋亡率没有观察到差异。在p53 + / +细胞中观察到端粒酶活性降低,而在p53-/-细胞中端粒酶活性升高。结果表明,虽然端粒酶活性和G1细胞周期阻滞取决于p53的状态,但G2阻滞和凋亡反应是通过不依赖p53的途径来促进的。

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