Journal article

AMPK beta 1 reduces tumor progression and improves survival in p53 null mice

Vanessa P Houde, Sara Donzelli, Andrea Sacconi, Sandra Galic, Joanne A Hammill, Jonathan L Bramson, Robert A Foster, Theodoros Tsakiridis, Bruce E Kemp, Giuseppe Grasso, Giovanni Blandino, Paola Muti, Gregory R Steinberg



The AMP-activated protein kinase (AMPK) is a heterotrimeric protein complex that is an important sensor of cellular energy status. Reduced expression of the AMPK β1 isoform has been linked to reduced survival in different cancers, but whether this accelerates tumor progression and the potential mechanism mediating these effects are not known. Furthermore, it is unknown whether AMPK β1 is implicated in tumorigenesis, and if so, what tissues may be most sensitive. In the current study, we find that in the absence of the tumor suppressor p53, germline genetic deletion of AMPK β1 accelerates the appearance of a T-cell lymphoma that reduces lifespan compared to p53 deficiency alone. This increase..

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Funding Acknowledgements

We thank Drs Rebecca Ford, Emmanuel Denou, and Toran Sanli for technical assistance and Associate Professor Carl Walkley, St Vincent's Institute, for reviewing the manuscript. This study was supported by grants from the Canadian Cancer Society Research and Innovation Fund to GRS. GRS is a Canada Research Chair in Metabolism and Obesity and the J. Bruce Duncan Chair in Metabolic Diseases. BEK, SG, and GRS are supported by grants from the National Health and Medical Research Council (NHMRC) and in part by the Victorian Government's Operational Infrastructure Support Program.