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Hepatoeellular carcinoma (HCC) is one of the most common and aggressive tumors in the world.The chronic infection of hepatitis B virus (HBV) is a major risk factor.As an oncoprotein encoded by HBV, HBV X protein (HBx), is involved in the pathogenesis of HBV-assoeiated liver diseases.HBx as a trans-aetivation factor is able to drive multiple signaling networks.Our laboratory has been investigating the mechanism by which HBx induces hepatoearcinogenesis by molecular biology and bio-informatics.Our data show that HBx is able to active oncoprotein, microRNA, long noncoding RNA (IncRNA) to promote the development of HCC.We found that HBx modulates oncogene YAP via CREB to promote growth of hepatoma cells.LncRNA HULC contributes to HBx-related hepatoearcinogenesis through suppressing p1 8.HBx up-regulates Lin28A/Lin28B through Sp-1/c-Myc to enhance the proliferation of hepatoma cells.HBx activates CD59 involving DNA binding and let-7i in protection of hepatoma and hepatic cells from complement attack.HBx drives multiple cross-talk cascade loops involving NF-kB, 5-LOX, OPN and Capn4 to promote cell migration.Up-regulated microRNA-29a by HBx protein enhances hepatoma cell migration by targeting PTEN in cell culture model.Importantly, HBx integration in the genome of liver cells is involved in hepatocarcinogenesis via a recombination of HBx/Alu core sequence/subtelomeric DNA.Thus, we conclude that HBx drives multiple signaling networks to promote cell proliferation and migration.Therapeutically, HBx may serve as an important target in hepatoma.