c-Myc suppression of miR-23a/b enhances mitochondrial glutaminase expression and glutamine metabolism

Ping Gao (), Irina Tchernyshyov, Tsung-Cheng Chang, Yun-Sil Lee, Kayoko Kita, Takafumi Ochi, Karen I. Zeller, Angelo M. De Marzo, Jennifer E. Van Eyk, Joshua T. Mendell and Chi V. Dang ()
Additional contact information
Ping Gao: Division of Hematology, Department of Medicine,
Irina Tchernyshyov: Division of Cardiology, Department of Medicine,
Tsung-Cheng Chang: McKusick-Nathans Institute of Genetic Medicine,
Yun-Sil Lee: McKusick-Nathans Institute of Genetic Medicine,
Kayoko Kita: Laboratory of Toxicology, Faculty of Pharmaceutical Sciences, Teikyo University, Sagamiko, Kanagawa 229-0195, Japan
Takafumi Ochi: Laboratory of Toxicology, Faculty of Pharmaceutical Sciences, Teikyo University, Sagamiko, Kanagawa 229-0195, Japan
Karen I. Zeller: Division of Hematology, Department of Medicine,
Angelo M. De Marzo: Departments of Pathology,
Jennifer E. Van Eyk: Division of Cardiology, Department of Medicine,
Joshua T. Mendell: McKusick-Nathans Institute of Genetic Medicine,
Chi V. Dang: Division of Hematology, Department of Medicine,

Nature, 2009, vol. 458, issue 7239, 762-765

Abstract: c-Myc links cancer to metabolism c-Myc is an oncogene involved in many forms of cancer. Proteomic analysis of human P-493 B lymphoma cells and PC3 prostate cancer cells shows that c-Myc regulates the microRNAs miR-23a and miR-23b to increase the expression of the mitochondrial enzyme glutaminase. This leads to enhanced glutamine metabolism and contributes to the metabolic changes in Myc-driven cancers.

Date: 2009
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DOI: 10.1038/nature07823

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