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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。
Genetically imprinted gene 10 (PEG10) is highly expressed in most hepatocellular carcinomas, and PEG10 and SIAH1 genes interact in hepatoma cells. Overexpression of PEG10 can inhibit SIAH1-mediated apoptosis and SIAH1 can significantly inhibit the expression of PEG10 Both expression and imbalance may participate in the formation of hepatocarcinoma by inhibiting apoptosis. Aberrant activation of Wnt / β-catenin signaling pathway plays an important role in the development of hepatocellular carcinoma. However, β-catenin, a key factor in SIAH1 degradation, induces hepatocellular apoptosis and growth arrest, Play an important role. Both PEG10 and β-catenin are closely related to SIAH1. The carcinogenicity of PEG10 may be partly attributed to the Wnt / β-catenin signaling pathway.