Insrr Regulates IFN-β through Regulation of Actin Cytoskeleton Pathway in Rat Hepatocellular Carcinoma

Abstract

Abstract Purpose:Hepatocellular carcinoma, caused by Hepatitis B Virus and Hepatitis C Virus infections and other factors, is one of the most common malignant tumors in the world. Interferon exerts its biological function by inducing the expression of hundreds of Interferon-stimulated genes in the host cells, which are responsible for inhibiting the replication, transcription, and other important processes of Hepatitis B Virus. The aim of this study was to find the proto-oncogenes or oncogenes that can regulate Interferon-β and the mechanism by which the genes regulate Interferon-β, and to identify targets for gene therapy for rat hepatocellular carcinoma. Methods: We induced hepatocellular carcinoma in rats by Diethylnitrosamine, and the development of hepatocellular carcinoma was inhibited by metformin, troxerutin, or a combination of metformin and troxerutin. The concentration of Interferon-β was detected and observed whether the level of Interferon-β was positively or negatively related to hepatocellular carcinoma. Transcriptome sequencing and RT-PCR was performed to finally determine the target genes that regulate Interferon-β and their mechanisms of action. Results: Various pathological and immunological results showed that we successfully induced and inhibited rat hepatocellular carcinoma. Insrr was identified as the genes capable of regulating Interferon-β by transcriptome sequencing and RT-PCR with statistical significance. Conclusion: Our study reveals the mechanism by which Insrr regulates Interferon-β in HCC, and the regulation of actin cytoskeleton pathway may be a potential target for HCC treatment.