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Suppression of Bcl-xL Deamidation in Human Hepatocellular Carcinomas¹

Department of Molecular Therapeutics, Osaka University Graduate School of Medicine, Suita 565-0871, Japan [T. T.]; and Institute of Clinical Medicine and Research, Jikei University School of Medicine, Kashiwa 277-8567, Japan [H. T.]

Bcl-xL is an antiapoptotic member of the Bcl-2 family, which inhibits apoptosis initiated by various cellular stresses, and has a pivotal role in the survival of tumor cells. Researchers have previously observed elevated expression of Bcl-xL in some human malignancies. In this study, we present evidence that human Bcl-xL is deamidated at asparagines 52 and 66 and that the rate of Bcl-xL deamidation is significantly lower in hepatocellular carcinomas than in normal or adjacent nontumor liver tissues. Because protein deamidation of Bcl-xL imports a complete "loss of function" of this antiapoptotic molecule, the present study indicates that tumor cells may acquire resistance to apoptosis and a survival advantage by suppressing deamidation as well as by increasing the expression of Bcl-xL. Thus, suppression of Bcl-xL deamidation may play a critical role in the regulation of cell death by apoptosis.

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