Liver cancer is a major contributor to cancer-related death with poor survival for sufferers. Meanwhile, Hepatic B virus X protein (HBx) and XB130 are likely to participate in the pathogenesis of liver cancer. However, the detailed mechanism of HBx/XB130 in liver cancer remains to be further investigated. Our study explored the effects of HBx/XB130 on liver cancer progression. HBx and XB130 expression was detected by reverse transcription quantitative polymerase chain reaction (RT-qPCR) and Western blot. Overexpression of HBx and XB130 was found in liver cancer tissues and cells. Mechanistic study revealed that HBx could bind to and positively regulate XB130 in HepG2 cells. Subsequently, HBx expression was knocked down, while XB130 was overexpressed in HepG2 cells in order to observe the specific role of HBx/XB130 in liver cancer in vitro. Results of CCK-8, Transwell, wound healing, and colony formation assays suggested that HBx could mediate biological function of HepG2 cells by activating the XB130-mediated PI3K/AKT pathway. In summary, our data illustrate that inhibition of HBx effectively suppressed proliferation and metastasis and induced apoptosis of liver cancer cells, which might be partially reversed by XB130. HBx and XB130 may be potential targets for liver cancer pathogenesis.

中文翻译：

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HBx 的下调抑制了 HepG2 细胞的增殖、迁移和侵袭

肝癌是癌症相关死亡的主要原因，患者的生存率很低。同时，乙肝病毒X蛋白（HBx）和XB130可能参与肝癌的发病。然而，HBx/XB130 在肝癌中的详细机制仍有待进一步研究。我们的研究探讨了 HBx/XB130 对肝癌进展的影响。通过逆转录定量聚合酶链反应 (RT-qPCR) 和蛋白质印迹检测 HBx 和 XB130 表达。在肝癌组织和细胞中发现了HBx和XB130的过度表达。机理研究表明，HBx 可以结合并积极调节 HepG2 细胞中的 XB130。随后，HBx 表达被敲低，而 XB130 在 HepG2 细胞中过表达，以观察 HBx/XB130 在肝癌中的具体作用体外。CCK-8、Transwell、伤口愈合和集落形成试验的结果表明，HBx 可以通过激活 XB130 介导的 PI3K/AKT 通路来介导 HepG2 细胞的生物学功能。总之，我们的数据表明抑制 HBx 可有效抑制肝癌细胞的增殖和转移并诱导其凋亡，这可能会被 XB130 部分逆转。HBx 和 XB130 可能是肝癌发病机制的潜在靶点。