PRES1 CONTRIBUTES IN HEPATOCARCINOGENESIS IN PATIENTS WITH HBV INFECTION

肝纤维化的发展导致肝衰竭、肝细胞癌、食管静脉曲张和自发性腹膜炎，这些是肝硬化中危及生命的并发症。然而，慢性B型肝炎病毒感染的患者偶尔会在非肝硬化的肝脏中发展为肝细胞癌。因此，推测慢性B型肝炎病毒感染的肝癌发生过程中可能存在一些未知的机制。HBX蛋白是这些因子的候选者之一。在这里，我们第一次表明，HBV前S1是另一个候选蛋白参与这种机制。它影响了EGF-EGFR信号通路的前馈机制，深刻地参与了肝癌的发生。这一新的证据是重要的，因为它可能有助于阐明复杂的肝癌发生机制，并在不久的将来找到肝癌的治疗途径。

Development of liver fibrosis results in hepatic failure, hepatocellular carcinoma, esophageal varices, and spontaneous peritonitis, which are life-threatening complications in liver cirrhosis. However, patients with chronic hepatitis B virus infection occasionally develop hepatocellular carcinoma in non-cirrhotic liver. Therefore, some unknown mechanisms are assumed to be involved in the process of hepatocarcinogenesis in chronic hepatitis B virus infection. HBX protein has been one of the candidates of such factors. Here we showed for the first time that HBV preS1 is another candidate protein involved in such a mechanism. It affects the feedforward mechanism of EGF-EGFR signalling pathway profoundly involved hepatocarcinogenesis. This novel evidence is important since it may contribute to elucidate the complex mechanism of hepatocarcinogenesis and to find a therapeutic path of hepatocarcinoma in the near future.