Department of Pharmacology and The Penn State Cancer Institute, The Pennsylvania State University College of Medicine, Milton S. Hershey Medical Center, 500 University Drive, Hershey, PA 17033, USA.
FEBS Lett. 2010 Aug 20;584(16):3519-24. doi: 10.1016/j.febslet.2010.07.018. Epub 2010 Jul 16.
We reported a novel interaction between Beclin 1, a key regulator of autophagy, and survivin, a member of the inhibitor of apoptosis protein family. We found that knock-down of Beclin 1 down-regulated survivin protein, and the turnover rate of survivin was increased when Beclin 1 expression was silenced. Knock-down of Beclin 1 sensitized glioma cells to TRAIL-induced apoptosis, and introduction of survivin antagonized the sensitizing effect, suggesting that down-regulation of survivin mediates the enhanced sensitivity to TRAIL-induced apoptosis. These results demonstrate a novel interaction between Beclin 1 and survivin, and may provide a potential mechanism underlying the cross-talk between autophagy and apoptosis.
我们报道了自噬关键调节因子 Beclin 1 与凋亡抑制蛋白家族成员 survivin 之间的一种新的相互作用。我们发现,Beclin 1 的敲低降低了 survivin 蛋白的表达,并且当 Beclin 1 表达被沉默时 survivin 的周转率增加。Beclin 1 的敲低使神经胶质瘤细胞对 TRAIL 诱导的凋亡敏感,而 survivin 的引入拮抗了这种敏化作用,表明 survivin 的下调介导了对 TRAIL 诱导的凋亡的增强敏感性。这些结果表明 Beclin 1 和 survivin 之间存在新的相互作用,并且可能为自噬和凋亡之间的串扰提供潜在的机制。