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为了探索结直肠癌细胞HCT116抗TRAIL诱导凋亡的分子机制,本课题以其抗性细胞HCT116 bax~(-/-)为实验对象进行了研究.通过利用目前最热的基因定点编辑技术Clustered regularly interspaced short palindromic repeats(CRISPR)/CRISPR-associated(Cas)9系统将HCT116bax~(-/-)的XIAP(X-linked inhibitor of apoptosis protein)基因彻底敲除后,用TRAIL处理,发现其恢复了对TRAIL的敏感,形态学发生了明显凋亡,而且western blot检测显示PARP蛋白发生了完全剪切.由此证明敲除XIAP基因能克服HCT116 bax~(-/-)对TRAIL的抗性.这些发现对肿瘤细胞抗TRAIL的分子机理研究以及肿瘤的个性化治疗有非常重要的意义.
In order to explore the molecular mechanism of anti-TRAIL-induced apoptosis in colorectal cancer cell line HCT116, the present study was carried out using HCT116 bax ~ (- / -) as an experimental cell.Through the use of the hottest gene-editing technique Clustered Regular After knockdown of HCT116bax ~ (- / -) XIAP (X-linked inhibitor of apoptosis protein) gene by TRAIL, we found that it restored the TRAIL sensitive and morphologically significant apoptosis, and western blot showed complete cleavage of PARP protein.Therefore, knocking out XIAP gene can overcome the resistance of HCT116 bax ~ (- / -) to TRAIL.These findings The molecular mechanism of anti-TRAIL tumor cells as well as the personalized treatment of cancer is of great significance.