自噬
安普克
活性氧
细胞凋亡
细胞生物学
PI3K/AKT/mTOR通路
癌细胞
线粒体
化学
线粒体ROS
程序性细胞死亡
癌症
信号转导
生物
生物化学
磷酸化
蛋白激酶A
遗传学
作者
Ke Zhang,Xingtao Zhou,Junqiao Wang,Y. Zhou,Wucheng Qi,Haihong Chen,Shaoping Nie,Mingyong Xie
标识
DOI:10.1016/j.carbpol.2021.118018
摘要
The homeostasis between mitochondrial function and autophagy is crucial to the physiological activity of cancer cells, and its mechanism is conducive to the development of anti-tumor drugs. Here, we aimed to explore the effect and mechanism of Dendrobium officinale polysaccharide (DOP) on colon cancer cell line CT26. Our data showed that DOP significantly inhibited the proliferation of CT26 cells and elevated autophagy level. Moreover, DOP disrupted mitochondrial function through increasing reactive oxygen species (ROS) and reducing mitochondrial membrane potential (MMP), thereby impairing ATP biosynthesis, which activated AMPK/mTOR autophagy signaling. Intriguingly, the further experiments demonstrated that DOP-induced cytotoxicity, excessive autophagy and mitochondrial dysfunction were reversed after CT26 cells pretreated with antioxidant (N-acetyl-l-cysteine). Herein, these findings implied that DOP-induced mitochondrial dysfunction and cytotoxic autophagy repressed the propagation of CT26 cells via ROS-ATP-AMPK signaling, providing a new opinion for the study of antineoplastic drugs.
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