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Oxidative Medicine and Cellular Longevity
Volume 2014 (2014), Article ID 504953, 10 pages
Research Article

Insulin Regulates Glucose Consumption and Lactate Production through Reactive Oxygen Species and Pyruvate Kinase M2

1Department of Pathology, State Key Lab of Reproductive Medicine, Cancer Center, Nanjing Medical University, Nanjing 210029, China
2Department of Pathology, Anhui Medical University, Hefei 230032, China
3Department of Oncology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China
4Department of Pathology, Anatomy and Cell Biology, Thomas Jefferson University, Philadelphia, PA 19107, USA

Received 12 February 2014; Accepted 11 April 2014; Published 8 May 2014

Academic Editor: Jinxiang Zhang

Copyright © 2014 Qi Li et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Although insulin is known to regulate glucose metabolism and closely associate with liver cancer, the molecular mechanisms still remain to be elucidated. In this study, we attempt to understand the mechanism of insulin in promotion of liver cancer metabolism. We found that insulin increased pyruvate kinase M2 (PKM2) expression through reactive oxygen species (ROS) for regulating glucose consumption and lactate production, key process of glycolysis in hepatocellular carcinoma HepG2 and Bel7402 cells. Interestingly, insulin-induced ROS was found responsible for the suppression of miR-145 and miR-128, and forced expression of either miR-145 or miR-128 was sufficient to abolish insulin-induced PKM2 expression. Furthermore, the knockdown of PKM2 expression also inhibited cancer cell growth and insulin-induced glucose consumption and lactate production, suggesting that PKM2 is a functional downstream effecter of insulin. Taken together, this study would provide a new insight into the mechanism of insulin-induced glycolysis.