Dendrobium Officinale Polysaccharide Triggers Mitochondrial Disorder to Induce Colon Cancer Cell Death Via ROS-AMPK-autophagy Pathway

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.