硒代半胱氨酸
细胞凋亡
活性氧
细胞生物学
癌细胞
DNA损伤
生物
信号转导
DNA断裂
程序性细胞死亡
化学
分子生物学
生物化学
癌症
DNA
遗传学
半胱氨酸
酶
作者
Kaiying Zhang,Jingyong Su,Danyang Chen,Binger Lin,Yucan Wu,Yibing Wang,J. van der Lei,Zheng Ren,Bing Zhu,Yinghua Li
标识
DOI:10.1007/s11033-022-07655-z
摘要
Currently, Liver cancer is the fifth most common tumor and the second most important reason for cancer-related death in the world. However, there are still many limitations of the clinical treatment of liver cancer, and new treatment options are clearly needed. Fortunately, studies have shown that L-Selenocysteine has a certain effect on cancer. This study was to investigate the effects of L-Selenocysteine on the inhibition of cell proliferation and the promotion of apoptosis of HepG-2 cells through ROS mediated fine signaling pathway.CCK-8 assay was applied to evaluating the cytotoxic effect of L-Selenocysteine on HepG-2 cells. Electron microscopy, flow cytometry and Western Blot was utilization in further researching cells signaling pathways.The growth of HepG-2 cells was inhibited by L-selenocysteine treatment in a dose-dependent manner. The cell viability decreased to 52.20%, 43.20% and 30.83% under the treatment of 4, 8, 16 µM L-selenocysteine, respectively. L-Selenocysteine had higher cytotoxicity towards HepG-2 cells than normal cells. L-Selenocysteine can induce the apoptosis of HepG-2 cells by increasing the DNA fragmentation, and activating the Caspase-3. In addition, it was found that the mechanism of the induction to HepG-2 cell apoptosis by L-Selenocysteine was closely related to the overproduction of ROS and promoted apoptosis through the Bcl-2 signaling pathway.Our data suggest that L-selenocysteine may cause mitochondrial damage and subsequently stimulate ROS production. ROS can damage cellular DNA and mediate the production of Casapase-8, Bid, Bcl-2 and other proteins, affecting downstream signaling pathways, and ultimately induced apoptosis.
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