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[Cancer Research 63, 3043-3048, June 15, 2003]
© 2003 American Association for Cancer Research

Advances in Brief

Involvement of PEG10 in Human Hepatocellular Carcinogenesis through Interaction with SIAH11

Hiroshi Okabe, Seiji Satoh, Yoichi Furukawa, Tatsushi Kato, Suguru Hasegawa, Yumi Nakajima, Yoshio Yamaoka and Yusuke Nakamura2

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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