乙型肝炎表面抗原
基因敲除
乙型肝炎病毒
HBeAg
基因沉默
癌症研究
分子生物学
医学
生物
病毒学
细胞培养
病毒
生物化学
基因
遗传学
作者
Bin Li,Yonggang Li,Shuhua Li,Hongwei Li,Ling Liu,Yu H
出处
期刊:PubMed
日期:2022-01-01
卷期号:14 (4): 2199-2211
被引量:3
摘要
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).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).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.Circ_MTM1 could serve as a promoter in HBV-related LF through miR-122-5p/IL7R axis.
科研通智能强力驱动
Strongly Powered by AbleSci AI