TRIM24的高表达促进胃癌细胞的生长并且通过Akt信号通路导致耐药

来源 :第9届全国胃癌学术会议暨第二届阳光长城肿瘤学术会议 | 被引量 : 0次 | 上传用户:liongliong603
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  目的:近年来研究表明,TRIM24在多种肿瘤的发生、发展中扮演着不同的角色.然而,在胃癌中TRIM24的作用还不清楚.方法:通过免疫组化分析法,在85例胃癌患者中研究TRIM24的表达情况.我们在低内源性表达SGC-7901细胞系中过度TRIM24,并且在高内源性表达TRIM24的MKN-1细胞系进行siRNA基因敲除.结果:实验证明,TRIM24在37/85例胃癌组织中呈现高表达.TRIM24的表达与患者的临床分期呈正相关.MTT法检测结果在细胞增殖时TRM24过表达,而基因敲除会导致细胞增殖率的降低.TRIM24的过表达也抑制5-FU诱导的细胞凋亡.进一步的分析表明TRIM24能够调控cyclin D1,cyclin E和Bcl-2的表达.此外,我们发现TRIM24能够调控Akt信号传导通路的活性.Akt信号传导通路的抑制剂LY294002能够部分逆转TRIM24对细胞增殖,细胞周期蛋白,Bcl-2的影响.结论:我们的研究表明TRIM24的异常表达有利于胃癌细胞的恶性生长,并且抑制药物诱导的细胞凋亡,可能通过上调Akt信号传导通路的细胞周期和Bcl蛋白等.
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