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Laforin Confers Cancer Resistance to Energy Deprivation–Induced Apoptosis

¹ Division of Immunotherapy, Section of General Surgery and ² Department of Surgery, Program of Molecular Mechanism of Diseases and Comprehensive Cancer Center, University of Michigan Ann Arbor, Michigan and ³ Department of Pathology, The Ohio State University, Columbus, Ohio

Requests for reprints: Pan Zheng or Yang Liu, Division of Immunotherapy, Section of General Surgery and Department of Surgery, Program of Molecular Mechanism of Diseases and Comprehensive Cancer Center, University of Michigan, Ann Arbor, MI 48109. E-mail: panz{at}umich.edu or yangl{at}umich.edu.

Key Words: apoptosis • cancer therapy • energy metabolism

A long-standing but poorly understood observation in experimental cancer therapy is the heterogeneity in cancer susceptibility to energy deprivation. Here, we show that the hexose kinase inhibitor 2-deoxyglucose (2-dG) preferentially kills cancer cells with defective laforin expression and significantly increases the survival of mice with aggressive lymphoma due to a genetic defect of the laforin-encoding Epm2a gene. Normal cells from Epm2a^–/– mice also had greatly increased susceptibility to 2-dG. Thus, laforin is a novel regulator for cellular response to energy deprivation and its defects in cancer cells may be targeted for cancer therapy. [Cancer Res 2008;68(11):4039–43]

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