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首页> 外文期刊>Cell biology international. >Bcl-2 down-regulation by small interfering RNA induces Beclin1-dependent autophagy in human SGC-7901 cells
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Bcl-2 down-regulation by small interfering RNA induces Beclin1-dependent autophagy in human SGC-7901 cells

机译：Bcl-2下调的小干扰RNA诱导人SGC-7901细胞中Beclin1依赖性自噬。

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摘要

While Bcl-2 protein is involved in the regulation of apoptosis, recent research showed that Beclinl, described as the essential autophagy effector and haploinsufficient tumor suppressor, was originally isolated as a Bcl-2 interacting protein. Beclinl interacts with Bcl-2 through a BH3 domain; nevertheless, the function of the anti-apoptotic gene, Bcl-2, in autophagy is not well understood. We explored the role of Bcl-2 in autophagy in human SGC-7901 cells in which Bcl-2 is overexpressed. Knockdown of Bcl-2 by small interfering RNA in human SGC-7901 cells downregulated Bcl-2 protein levels ~82% and induced autophagy. Beclinl protein, the first identified autophagy gene product, was induced by as much as 58%. Transmission electron microscopy and DNA fragmentation assay showed that autophagy was enhanced, but not apoptosis, in Bcl-2 siRNA treated cells. The results provide evidence that knockout the anti-apoptotic gene Bcl-2 induces autophagy in SGC-7901 cells and Bcl-2 specific siRNA may be used as a potential therapeutic strategy in gastric cancer cells that overexpress Bcl-2.
机译：虽然Bcl-2蛋白参与细胞凋亡的调控，但最近的研究表明，被描述为必不可少的自噬效应物和单倍体不足的肿瘤抑制物的Beclinl最初是作为Bcl-2相互作用蛋白被分离出来的。 Beclinl通过BH3结构域与Bcl-2相互作用;但是，抗凋亡基因Bcl-2在自噬中的功能尚不十分清楚。我们探索了Bcl-2在Bcl-2过表达的人SGC-7901细胞自噬中的作用。在人SGC-7901细胞中通过小分子干扰RNA抑制Bcl-2的表达下调了Bcl-2的蛋白质水平〜82％，并诱导了自噬。 Beclinl蛋白是第一个被鉴定为自噬的基因产物，被诱导多达58％。透射电子显微镜和DNA片段测定表明，在Bcl-2 siRNA处理的细胞中，自噬得到增强，但没有凋亡。结果提供了证据，敲除抗凋亡基因Bcl-2在SGC-7901细胞中诱导自噬，并且Bcl-2特异性siRNA可能被用作过表达Bcl-2的胃癌细胞的潜在治疗策略。

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