Journal
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume 437, Issue 2, Pages 225-231Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2013.06.043
Keywords
p53; miR-34a; Glycolysis; HK; GPI; PDK1
Categories
Funding
- National Research Foundation of Korea (NRF)
- Korea government (MSIP) [2012R1A3 A2048767]
- Mid-Career Research Program
- National Research Foundation of Korea [NRF-2007-0056786, NRF-2010-0007643]
- World Class University Program of the MEST
- NRF [R31-2008-000-10103-0]
- National R&D Program for Cancer Control, Ministry of Health Welfare [0720460]
- Korea Health Promotion Institute [0720460] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
- National Research Foundation of Korea [R31-2012-000-10103-0, 2007-0056786, 2010-0007643, 2012R1A3A2048767] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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Cancer cells rely mainly on glycolysis rather than mitochondrial respiration for energy production, which is called the Warburg effect. p53 mutations are observed in about half of cancer cases, and p53 controls the cell cycle and cell death in response to cellular stressors. p53 has been emphasized as a metabolic regulator involved in glucose, glutamine, and purine metabolism. Here, we demonstrated metabolic changes in cancer that occurred through p53. We found that p53-inducible microRNA-34a (miR-34a) repressed glycolytic enzymes (hexokinase 1, hexokinase 2, glucose-6-phosphate isomerase), and pyruvate dehydrogenase kinase 1. Treatment with an anti-miR-34a inhibitor relieved the decreased expression in these enzymes following DNA damage. miR-34a-mediated inhibition of these enzymes resulted in repressed glycolysis and enhanced mitochondrial respiration. The results suggest that p53 has a miR-34a-dependent integrated mechanism to regulate glucose metabolism. (C) 2013 Elsevier Inc. All rights reserved.
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