HnRNP proteins controlled by c-Myc deregulate pyruvate kinase mRNA splicing in cancer

Charles J. David, Mo Chen, Marcela Assanah, Peter Canoll and James L. Manley ()
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Charles J. David: Columbia University, New York, New York 10027, USA
Mo Chen: Columbia University, New York, New York 10027, USA
Marcela Assanah: Columbia University, New York, New York 10032, USA
Peter Canoll: Columbia University, New York, New York 10032, USA
James L. Manley: Columbia University, New York, New York 10027, USA

Nature, 2010, vol. 463, issue 7279, 364-368

Abstract: Alternative splicing in cancer cells Cancer cells avidly take up glucose and convert it to lactate while eschewing oxidative phosphorylation. This phenomenon is critical for maximal tumorigenicity, and is in part explained by the almost universal reversion of tumours to the embryonic form of pyruvate kinase, PKM2. Here, David et al. now show that aberrant expression of the splicing factors PTB, hnRNPA1 and hnRNPA2, which are themselves regulated by the c-Myc oncogene, is responsible for the PKM1 to PKM2 switch in cancer. This work adds to our understanding of alternative splicing and its role in cancer cell growth.

Date: 2010
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DOI: 10.1038/nature08697

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