PEG10基因与Wnt/β-catenin信号通路在肝癌发病机制中的相互关系

The Interaction of PEG10 gene with the Wnt/beta-catenin Signaling Pathway in the Pathogenesis of HCC

遗传印记基因10(PEG10)在绝大多数肝癌中特异性高表达,PEG10和SIAH1基因在肝癌细胞中相互作用,过表达的PEG10可抑制SIAH1介导的细胞凋亡,同时SIAH1可显著抑制PEG10的表达,失平衡的二者可能通过抑制细胞凋亡参与肝癌形成。Wnt/β-catenin信号通路的异常激活在肝癌形成中起重要作用;而SIAH1降解该通路的关键因子β-连环素(β-catenin),诱导肝癌的细胞凋亡和生长停滞,在抑制肝癌形成中起重要作用。PEG10和β-catenin均与SIAH1密切联系,PEG10的致癌作用很可能部分归因于Wnt/β-catenin信号通路。

The paternally expressed gene 10（PEG10）is highly expressed in a great majority of hepatocellular carcinomas specifically.PEG10 can interact with SIAH1 in hepatoma carcinoma cells.The overexpression of PEG10 may decrease the apoptosis mediated by SIAH1,and SIAH1 may notably suppress the expression of PEG10.The imbalance between expression of PEG10 and SIAH1 may be involved in hepatocarcinogenesis through inhibition of apoptosis.The unusual activation of the canonical Wnt/beta-catenin signaling pathway plays an important role in hepatocarcinogenesis.SIAH1 may degrade beta-catenin that is the key factor in the signaling pathway,thus induces apoptosis and cell arrest and plays an important role in suppressing hepatocarcinogenesis.Both of the PEG10 and beta-catenin closely associate with SIAH1.It is very possible that the carcinogenesis of PEG10 partly ascribes to the Wnt/beta-catenin signaling pathway.