Involvement of PEG10 in human hepatocellular carcinogenesis through interaction with SIAH1.
Involvement of PEG10 in human hepatocellular carcinogenesis through interaction with SIAH1.
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发表时间：
2003-06
期刊：
影响因子：
11.2
通讯作者：
H. Okabe;S. Satoh;Y. Furukawa;Tatsushi Kato;Suguru Hasegawa;Y. Nakajima;Y. Yamaoka;Yusuke Nakamura-Yusuke
中科院分区：
文献类型：
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作者：
H. Okabe;S. Satoh;Y. Furukawa;Tatsushi Kato;Suguru Hasegawa;Y. Nakajima;Y. Yamaoka;Yusuke Nakamura-Yusuke
通过全基因组 cDNA 微阵列，我们发现父系表达基因 10 (PEG10) 在绝大多数肝细胞癌中高度表达，尽管其在正常肝细胞中不表达。 PEG10 的外源表达赋予致癌活性，用抑制 PEG10 的反义 S-寡核苷酸转染肝癌细胞会导致其生长受到抑制。其他实验表明，PEG10 蛋白与细胞凋亡介质 SIAH1 相关，并且 PEG10 的过度表达可减少 SIAH1 介导的细胞死亡。这些发现表明，开发抑制 PEG10 活性的药物可能成为治疗肝细胞癌的新方法。
Through a genome-wide cDNA microarray, we identified that the paternally expressed gene 10 (PEG10) was highly expressed in a great majority of hepatocellular carcinomas, although its expression was absent in normal liver cells. Exogenous expression of PEG10 conferred oncogenic activity and transfection of hepatoma cells with antisense S-oligonucleotides suppressing PEG10 resulted in their growth inhibition. Additional experiments revealed that PEG10 protein associated with SIAH1, a mediator of apoptosis, and that overexpression of PEG10 decreased the cell death mediated by SIAH1. These findings suggested that development of drug(s) inhibiting PEG10 activity could be a novel approach for the treatment of hepatocellular carcinomas.