Bin Li1, Yonggang Li1, Shuhua Li2, Hongwei Li2, Ling Liu2, Haiying Yu3. 1. Department of Pathogenic Biology, School of Basic Medicine, Jinzhou Medical University Jinzhou 121001, Liaoning, China. 2. Laboratory of Immunology and Pathogenic Biology, Experimental Teaching Center of Basic Medicine, Jinzhou Medical University Jinzhou 121001, Liaoning, China. 3. Laboratory of Ergology, Experimental Teaching Center of Basic Medicine, Jinzhou Medical University Jinzhou 121001, Liaoning, China.
Abstract
BACKGROUND AND OBJECTIVE: Hepatitis B virus (HBV) infection is the main reason for liver cirrhosis. The purpose of this research was to probe into the role and underlying mechanism of circ_myotubularin 1 (circ_MTM1) in HBV-related liver fibrosis (LF). METHODS: HBV surface antigen (HBsAg) and e antigen (HBeAg), as well as the levels of HBV DNA and HBV covalently closed circular DNA were measured by HBsAg and HBeAg ELISA kits or RT-qPCR. Western blot or immunohistochemistry assays were conducted to measure protein levels. The expression of circ_MTM1, microRNA-122-5p (miR-122-5p) and interleukin 7 receptor (IL7R) were measured using RT-qPCR. MTT and cell colony formation assays were performed to detect cell proliferation. In vivo assays were carried out to reveal the effect of circ_MTM1 silencing on the tumor growth in HBV-related hepatocellular carcinoma (HCC). RESULTS: Circ_MTM1 and IL7R were highly expressed, whereas miR-122-5p was lowly expressed in HBV-infected LX-2 cells. Circ_MTM1 knockdown inhibited the progression of HBV-related LF. Circ_MTM1 could target miR-122-5p to regulate the expression of IL7R by adsorbing miR-122-5p, thus mediating the progression of HBV-related LF. Circ_MTM1 silencing repressed cell proliferation of HepG2.2.15 cells and growth of HCC. CONCLUSION: Circ_MTM1 could serve as a promoter in HBV-related LF through miR-122-5p/IL7R axis. AJTR
BACKGROUND AND OBJECTIVE: Hepatitis B virus (HBV) infection is the main reason for liver cirrhosis. The purpose of this research was to probe into the role and underlying mechanism of circ_myotubularin 1 (circ_MTM1) in HBV-related liver fibrosis (LF). METHODS: HBV surface antigen (HBsAg) and e antigen (HBeAg), as well as the levels of HBV DNA and HBV covalently closed circular DNA were measured by HBsAg and HBeAg ELISA kits or RT-qPCR. Western blot or immunohistochemistry assays were conducted to measure protein levels. The expression of circ_MTM1, microRNA-122-5p (miR-122-5p) and interleukin 7 receptor (IL7R) were measured using RT-qPCR. MTT and cell colony formation assays were performed to detect cell proliferation. In vivo assays were carried out to reveal the effect of circ_MTM1 silencing on the tumor growth in HBV-related hepatocellular carcinoma (HCC). RESULTS: Circ_MTM1 and IL7R were highly expressed, whereas miR-122-5p was lowly expressed in HBV-infected LX-2 cells. Circ_MTM1 knockdown inhibited the progression of HBV-related LF. Circ_MTM1 could target miR-122-5p to regulate the expression of IL7R by adsorbing miR-122-5p, thus mediating the progression of HBV-related LF. Circ_MTM1 silencing repressed cell proliferation of HepG2.2.15 cells and growth of HCC. CONCLUSION: Circ_MTM1 could serve as a promoter in HBV-related LF through miR-122-5p/IL7R axis. AJTR