Liu Bo, Cheng Yan, Zhang Bo, Bian He-jiao, Bao Jin-ku
College of Life Sciences, State Key Laboratory of Oral Diseases, Sichuan University, Wuhou District, Chengdu 610064, China.
Cancer Lett. 2009 Mar 8;275(1):54-60. doi: 10.1016/j.canlet.2008.09.042. Epub 2008 Nov 17.
Polygonatum cyrtonema lectin (PCL), a mannose-binding lectin, has been reported to induce cytotoxicity and apoptosis. Herein, we demonstrated that PCL-induced apoptosis and autophagy in A375 cells. The apoptotic mechanism was that PCL treatment regulated Bax, Bcl-xL and Bcl-2 proteins, leading to mitochondrial depolarization, cytochrome c release and caspase activation. Subsequently, we found that PCL treatment abrogated glutathione antioxidant system and induced mitochondria to generate ROS accumulation, resulting in p38-p53 activation. Moreover, we confirmed that the ROS-p38-p53 pathway was involved in PCL-induced autophagy. In conclusion, these results indicate that PCL induces apoptosis and autophagy via a mitochondrial-mediated ROS-p38-p53 pathway.
黄精凝集素(PCL)是一种甘露糖结合凝集素,据报道可诱导细胞毒性和凋亡。在此,我们证明PCL可诱导A375细胞发生凋亡和自噬。凋亡机制是PCL处理调节了Bax、Bcl-xL和Bcl-2蛋白,导致线粒体去极化、细胞色素c释放和半胱天冬酶激活。随后,我们发现PCL处理破坏了谷胱甘肽抗氧化系统并诱导线粒体产生ROS积累,导致p38-p53激活。此外,我们证实ROS-p38-p53途径参与了PCL诱导的自噬。总之,这些结果表明PCL通过线粒体介导的ROS-p38-p53途径诱导凋亡和自噬。