Mitofusin2 Induces Cell Autophagy of Pancreatic Cancer through Inhibiting the PI3K/Akt/mTOR Signaling Pathway

Aim. Pancreatic canceris one of the most quickly fatal cancers around the world. Burgeoning researches have begun to prove that mitochondria play a crucial role in cancer treatment. Mitofusin2 ( Mfn2) plays an indispensable role in mitochondrial fusionand adjusting function. However, the role and underlying mechanisms of Mfn2on cell autophagy of pancreatic canceris still unclear. Our aim was to explore the effect of Mfn2on multiple biological functions involving cell autophagy in pancreatic cancer. Methods. Pancreatic cancercell line, Aspc-1, was treated with Ad- Mfn2overexpression. Western blotting, caspase-3 activity measurement, and CCK-8 and reactive oxygen species (ROS) assay were used to examine the effects of Mfn2on pancreatic cancerautophagy, apoptosis, cell proliferation, oxidative stress, and PI3K/Akt/mTOR signaling. The expression of tissue Mfn2was detected by immunohistochemical staining. Survival analysis of Mfn2was evaluated by OncoLnc. Results. Mfn2improved the expression of LC3-II and Bax and downregulated the expression of P62 and Bcl-2 in pancreatic cancercells. Meanwhile, Mfn2also significantly inhibited the expression of p-PI3K, p-Akt, and p-mTOR proteins in pancreatic cancercells. In addition, Mfn2inhibited pancreatic cancercell proliferation and ROS production. Assessment of Kaplan-Meier curves showed that Mfn2− pancreatic cancerhas a worse prognosis than Mfn2