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    AMPKα loss promotes KRAS-mediated lung tumorigenesis

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    Authors
    La Montagna, Manuela
    Shi, Lei
    Magee, Peter
    Sahoo, Sudhakar
    Fassan, M
    Garofalo, Michela
    Affiliation
    Transcriptional Networks in Lung Cancer Group, Cancer Research UK Manchester Institute, The University of Manchester, Manchester, UK.
    Issue Date
    2021
    
    Metadata
    Show full item record
    Abstract
    AMP-activated protein kinase (AMPK) is a critical sensor of energy status that coordinates cell growth with energy balance. In non-small cell lung cancer (NSCLC) the role of AMPKα is controversial and its contribution to lung carcinogenesis is not well-defined. Furthermore, it remains largely unknown whether long non-coding RNAs (lncRNAs) are involved in the regulation of AMPK-mediated pathways. Here, we found that loss of AMPKα in combination with activation of mutant KRASG12D increased lung tumour burden and reduced survival in KrasLSLG12D/+/AMPKαfl/fl mice. In agreement, functional in vitro studies revealed that AMPKα silencing increased growth and migration of NSCLC cells. In addition, we identified an AMPKα-modulated lncRNA, KIMAT1 (ENSG00000228709), which in turn regulates AMPKα activation by stabilizing the lactate dehydrogenase B (LDHB). Collectively, our study indicates that AMPKα loss promotes KRAS-mediated lung tumorigenesis and proposes a novel KRAS/KIMAT1/LDHB/AMPKα axis that could be exploited for therapeutic purposes.
    Citation
    La Montagna M, Shi L, Magee P, Sahoo S, Fassan M, Garofalo M. AMPKα loss promotes KRAS-mediated lung tumorigenesis. Cell Death Differ. 2021 May 26.
    Journal
    Cell Death and Differentiation
    URI
    http://hdl.handle.net/10541/624130
    DOI
    10.1038/s41418-021-00777-0
    PubMed ID
    34040167
    Additional Links
    https://dx.doi.org/10.1038/s41418-021-00777-0
    Type
    Article
    Language
    en
    ae974a485f413a2113503eed53cd6c53
    10.1038/s41418-021-00777-0
    Scopus Count
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    All Paterson Institute for Cancer Research

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