Radix Actinidiae chinensis induces autophagy in renal cell carcinoma 786-O and A498 cells by regulating PI3K/AKT/mTOR pathway

Abstract

Objective: Renal cell carcinoma (RCC) is a malignant tumor. This study investigated the mechanism of Radix Actinidiae chinensis (RAC) inducing autophagy in RCC cell.Methods: Cell viability and IC50 value in 786-O and A498 cells were detected by CCK8 assays. The proliferation, cell cycle, migration and invasion were detected by cloning, flow cytometry and cell invasion assays, respectively. The cell apoptosis, cycle, autophagy and related protein levels were detected by flow cytometry, AOPI assay and western blot, respectively. The number of autophagolysosomes was detected by electron microscopy. In addition, the proteins related to the PI3K/AKT/mTOR pathway were detected by western blot.Results: IC50 values of RAC in 786-O and A498 cells were 14.76 mg/mL and 13.09 mg/mL, respectively. RAC treatment reduced cell viability, proliferation, migration and invasion, blocked the S phase cells, and promoted apoptosis and autophagyin 786-O and A498 cells. It also increased the autophagy-related proteins LC3II/I and Beclin-1, and decreased the level of p62. In addition, RAC activated the levels of apoptosis-related proteins and reduce the levels of PI3K/AKT/mTOR pathway-related proteins. However, the addition of autophagy inhibitor 3-MA attenuated the effect of RAC on apoptosis, autophagy and the expression of related proteins in RCC cells.Conclusion: RAC can induce autophagy in RCC by blocking PI3K/AKT/mTOR pathway, to inhibit the progression of RCC cells.