亚砷酸钠
蛋白激酶B
细胞凋亡
MAPK/ERK通路
化学
PI3K/AKT/mTOR通路
细胞生物学
细胞色素c
p38丝裂原活化蛋白激酶
信号转导
活性氧
半胱氨酸蛋白酶3
生物化学
生物
程序性细胞死亡
砷
有机化学
作者
Wei‐Sheng Juan,Yi‐Fen Mu,Chia‐Yih Wang,Edmund Cheung So,Yan-Hua Lee,Sheng‐Che Lin,Bu‐Miin Huang
摘要
Arsenic compounds have been applied treating acute promyelocytic 1eukemia and solid tumors with brief mechanism investigations. In fact, we have demonstrated that sodium arsenite plus dimethylarsenic acid could activate apoptosis in MA-10 mouse Leydig tumor cells by inducing caspase pathways. However, detail underlying mechanisms how caspase cascade is regulated remains elusive. Therefore, the apoptotic mechanism of sodium arsenite plus dimethylarsenic acid were examined in MA-10 cells in this study. Our results reveal that Fas/FasL protein expressions were stimulated by sodium arsenite plus dimethylarsenic acid in MA-10 cells. In addition, reactive oxygen species (ROS) generation, cytochrome C release, Bid truncation, and Bax translocation were induced in MA-10 cells by arsenic compounds. Moreover, activation of p38, JNK and ERK1/2, MAPK pathways was stimulated while Akt phosphorylated levels and Akt expression were decreased by sodium arsenite plus dimethylarsenic in MA-10 cells. In conclusion, sodium arsenite and dimethylarsenic acid did activate MAPK pathway plus ROS generation, but suppress Akt pathway, to modulate caspase pathway and then induce MA-10 cell apoptosis.
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