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Involvement of PEG10 in Human Hepatocellular Carcinogenesis through Interaction with SIAH1¹

Laboratory of Molecular Medicine, Human Genome Center, Institute of Medical Science, The University of Tokyo, Tokyo 108-8639 [H. O., S. S., Y. F., T. K., S. H., Y. Nakaj., Y. Nakam.], and Department of Gastroenterological Surgery, Graduate School of Medicine, Kyoto University, Kyoto 606-8507 [H. O., S. S., T. K., Y. Y.], Japan

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.

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