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International Journal of Cell Biology
Volume 2013, Article ID 242513, 11 pages
Review Article

PKM2, a Central Point of Regulation in Cancer Metabolism

Nicholas Wong,1,2,3,4 Jason De Melo,1,2,3,4 and Damu Tang1,2,3,4

1Division of Nephrology, Department of Medicine, McMaster University, Hamilton, ON, L8S 4L8, Canada
2Division of Urology, Department of Surgery, McMaster University, Hamilton, ON, L8S 4L8, Canada
3Father Sean O'Sullivan Research Centre, St. Joseph's Healthcare Hamilton, Hamilton, ON, Canada L8N 4A6
4The Hamilton Center for Kidney Research, St. Joseph's Healthcare Hamilton, Hamilton, ON, Canada L8N 4A6

Received 2 December 2012; Revised 11 January 2013; Accepted 13 January 2013

Academic Editor: Claudia Cerella

Copyright © 2013 Nicholas Wong 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.


Aerobic glycolysis is the dominant metabolic pathway utilized by cancer cells, owing to its ability to divert glucose metabolites from ATP production towards the synthesis of cellular building blocks (nucleotides, amino acids, and lipids) to meet the demands of proliferation. The M2 isoform of pyruvate kinase (PKM2) catalyzes the final and also a rate-limiting reaction in the glycolytic pathway. In the PK family, PKM2 is subjected to a complex regulation by both oncogenes and tumour suppressors, which allows for a fine-tone regulation of PKM2 activity. The less active form of PKM2 drives glucose through the route of aerobic glycolysis, while active PKM2 directs glucose towards oxidative metabolism. Additionally, PKM2 possesses protein tyrosine kinase activity and plays a role in modulating gene expression and thereby contributing to tumorigenesis. We will discuss our current understanding of PKM2's regulation and its many contributions to tumorigenesis.