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  • Open Access

    REVIEW

    The Biological Function of Hepatitis B Virus X Protein in Hepatocellular Carcinoma

    Qiaodong Xu1, Songgang Gu1, Jiahong Liang, Zhihua Lin, Shaodong Zheng, Jiang Yan

    Oncology Research, Vol.27, No.4, pp. 509-514, 2019, DOI:10.3727/096504018X15278771272963

    Abstract Hepatocellular carcinoma (HCC) is one of the major malignant tumors that lead to death. Chronic hepatitis B virus infection is an important risk factor for HCC initiation. HBx protein, encoded by the HBV X gene, is a significant factor that promotes HBV-related HCC, although the exact molecular mechanism remains unclear. This article summarizes the pathological roles and related mechanisms of HBx in HCC. HBx plays a carcinogenic role by promoting cell proliferation, metastasis, and angiogenesis and inhibiting apoptosis in HCC. A detailed study of the biological functions of HBx will help to elucidate the mechanism of hepatocarcinogenesis and lead to… More >

  • Open Access

    ARTICLE

    MicroRNA 125a-5p Inhibits Cell Proliferation and Induces Apoptosis in Hepatitis B Virus-Related Hepatocellular Carcinoma by Downregulation of ErbB3

    Guoyun Li, Wei Zhang, Li Gong, Xiaoping Huang

    Oncology Research, Vol.27, No.4, pp. 449-458, 2019, DOI:10.3727/096504017X15016337254623

    Abstract MicroRNAs, a class of endogenous noncoding RNAs, regulate gene expression at the posttranscriptional level and thus take part in multiple biological processes. An increasing number of miRNAs have been found to be dysregulated in hepatocellular carcinoma (HCC) and are involved in liver tumorigenesis. In this study, miR- 125a-5p was found to be obviously downregulated much more in hepatitis B virus (HBV)-related HCC. To investigate the effects of miR-125a-5p, miR-125a-5p was overexpressed in HepG2.2.15 and HepG3X cells. The findings have indicated that overexpression of miR-125a-5p dramatically inhibited cell proliferation and induced cell apoptosis. Furthermore, overexpression of miR-125a-5p could significantly decrease the… More >

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