Blocking Adipor1 enhances radiation sensitivity in Hepatoma Carcinoma Cells

Abstract

In this study, we aimed to elucidate the roles of Adipor1 in radiation-induced cell death of Hepatocellular carcinoma (HCC). The human HCC cell line MHCC97-H and HepG2 were used to investigate the underlying mechanisms. Western blotting was used to detect protein expression, and flow cytometry was used to detect cell cycle and cell death. Orthotopic allograft HCC models were established in Rats. LV-Adipor1-RNAi virus were injected into the tumor before radiation. Such parameters as tumor diameter, blood indicators, and liver function index were detected.In vitro results indicated that Adipor1 knockdown enhanced radiation-induced cell death and DNA damage, and inhibited cell cycle arrest at the G2/M and autophagy, leading to increased apoptosis. In vivo experiments showed that Adipor1 knockdown increased radiosensitivity and significantly inhibited liver tumor growth, upregulated the number of red blood cell, platelet count and Hemoglobin content, decreased the content of ALT, AST and ALP. To sum up, Adipor1 blockade enhance therapeutic effects of radiation by inhibiting cell cycle arrest and autophagy, and promoting DNA damage and apoptosis in Hepatoma Carcinoma Cells.