| Objective: G protein-coupled receptors(GPCRs)are the largest known family of cell surface receptors that regulate signal transduction and transmission and control various physiological and pathological processes.The GPCRs regulator ARRBs play a role in the proliferation of cancer,however,the role of ARRBs in hepatocellular carcinogenesis is unknown.The purpose of this study was to verify the effects of ?-arrestin2 in hepatocellular cancer(HCC)and explore its potential target genes and the specific mechanisms by which it functions.Methods: The expression levels of ?-arrestin2 in cancer tissue and adjacent tissue samples from patients with hepatocellular carcinoma were detected by immunoblotting and immunohistochemistry.The content of the ?-arrestin2 in liver cancer and human hepatocytes cell lines were also detected by real-time fluorescent quantitative PCR and Western blot.By transient transfection techniques,CCK-8 was used to detect the proliferation of transfected cells,and Transwell was used to evaluate the invasiveness of transfected cells.Finally,Western blot experiments were used to verify the ?-arrestin2 signaling pathway.Results: The content of ?-arrestin2 in cancer tissues of patients with hepatocellular carcinoma was higher than that in adjacent tissues,and in vitro,hepatoma cell lines were highly expressed compared with normal hepatocytes.Overexpression and inhibition of ?-arrestin2 was used to verify its promotion of hepatocellular carcinoma cell proliferation and invasion.In addition,it was verified that ?-arrestin2 can phosphorylate Akt,leading to high expression of PCNA,thereby promoting the proliferation of hepatoma cells.Conclusions: This study shows that ?-arrestin2 is highly expressed in hepatocellular carcinoma.High expression of ?-arrestin2 promotes the proliferation and invasion of hepatocellular carcinoma cells,and interacts with Akt,which promotes the phosphorylation of Akt and leads to the malignant proliferation of hepatocytes. |
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