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RBM5蛋白调控c-FLIP差异性剪切及其抑制A549增殖的研究 被引量:2

RBM5 regulate the alternative splicing of c-FLIP and inhibits the proliferation of A549
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摘要 本文试探讨RBM5蛋白对肺腺癌细胞A549增殖的影响及其作用机制,以期为开辟肺癌基因治疗新途径提供帮助.本研究构建了表达RBM5基因的真核表达载体,并转染A549细胞株,增强其中该基因的表达量.采用RT-PCR检测转染后A549细胞中c-FLIP基因不同剪切体的表达量,并绘制生长曲线.结果表明,RBM5基因在A549细胞中的高表达,可以调控c-FLIP的差异剪切,减少c-FLIPs的表达量,激活细胞程序化死亡相关通路,抑制肺腺癌细胞恶性增殖. The aim of this study is to observe the effect of RBM5 on the proliferation of A549 cells, sequentially to explore the molecule mechanisms and novel gene therapy strategy of lung cancer. In this article, a RBM5 eukaryotic expression vector was constructed and transfected into A549 cells. The expression of c-FLIPL and c-FLIPs were detected by RT-PCR. Growth rate of A549 cells was calculated through cell counting. The results suggest that up-regulating RBM5 can inhibit the expression of the antiapoptotic c-FLIPs isoform and cell growth.
出处 《四川大学学报(自然科学版)》 CAS CSCD 北大核心 2010年第4期911-915,共5页 Journal of Sichuan University(Natural Science Edition)
基金 教育部博士点基金(20070610170) 国家自然科学基金重大研究计划(90919005) 科技部科技重大专项(2009ZX09103-698)
关键词 细胞程序化死亡 恶性增殖 半定量PCR RBM5 C-FLIP 差异性剪切 apoptosis, malignant proliferation, semi-quantitive RT-PCR, RBM5pro, c-FLIP, alternative splicing
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参考文献16

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