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

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    14
    Author
    Houde, VP; Donzelli, S; Sacconi, A; Galic, S; Hammill, JA; Bramson, JL; Foster, RA; Tsakiridis, T; Kemp, BE; Grasso, G; ...
    Date
    2017-09-01
    Source Title
    Molecular Oncology
    Publisher
    WILEY
    University of Melbourne Author/s
    Kemp, Bruce; Steinberg, Gregory; Galic, Sandra
    Affiliation
    Medicine and Radiology
    Metadata
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    Document Type
    Journal Article
    Citations
    Houde, V. P., Donzelli, S., Sacconi, A., Galic, S., Hammill, J. A., Bramson, J. L., Foster, R. A., Tsakiridis, T., Kemp, B. E., Grasso, G., Blandino, G., Muti, P. & Steinberg, G. R. (2017). AMPK beta 1 reduces tumor progression and improves survival in p53 null mice. MOLECULAR ONCOLOGY, 11 (9), pp.1143-1155. https://doi.org/10.1002/1878-0261.12079.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/259666
    DOI
    10.1002/1878-0261.12079
    Abstract
    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 increased tumorigenesis is linked to increases in interleukin-1β (IL1β), reductions in acetyl-CoA carboxylase (ACC) phosphorylation, and elevated lipogenesis. Collectively, these data indicate that reductions in the AMPK β1 subunit accelerate the development of T-cell lymphoma, suggesting that therapies targeting this AMPK subunit or inhibiting lipogenesis may be effective for limiting the proliferation of p53-mutant tumors.

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