Circ_MTM1 knockdown inhibits the progression of HBV-related liver fibrosis via regulating IL7R expression through targeting miR-122-5p.

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.