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    A KRAS-responsive long non-coding RNA controls microRNA processing

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    Authors
    Shi, Lei
    Magee, Peter
    Fassan, M.
    Sahoo, Sudhakar
    Leong, Hui Sun
    Lee, Dave
    Sellers, Robert
    Brullé-Soumaré, L.
    Cairo, S.
    Monteverde, Tiziana
    Volinia, S.
    Smith, Duncan D
    Di Leva, G.
    Galuppini, F.
    Paliouras, Athanasios R
    Zeng, Kang
    O'Keefe, R.
    Garofalo, Michela
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    Affiliation
    Transcriptional Networks in Lung Cancer Group, Cancer Research UK Manchester Institute, University of Manchester, Mancheste
    Issue Date
    2021
    
    Metadata
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    Abstract
    Wild-type KRAS (KRASWT) amplification has been shown to be a secondary means of KRAS activation in cancer and associated with poor survival. Nevertheless, the precise role of KRASWT overexpression in lung cancer progression is largely unexplored. Here, we identify and characterize a KRAS-responsive lncRNA, KIMAT1 (ENSG00000228709) and show that it correlates with KRAS levels both in cell lines and in lung cancer specimens. Mechanistically, KIMAT1 is a MYC target and drives lung tumorigenesis by promoting the processing of oncogenic microRNAs (miRNAs) through DHX9 and NPM1 stabilization while halting the biogenesis of miRNAs with tumor suppressor function via MYC-dependent silencing of p21, a component of the Microprocessor Complex. KIMAT1 knockdown suppresses not only KRAS expression but also KRAS downstream signaling, thereby arresting lung cancer growth in vitro and in vivo. Taken together, this study uncovers a role for KIMAT1 in maintaining a positive feedback loop that sustains KRAS signaling during lung cancer progression and provides a proof of principle that interfering with KIMAT1 could be a strategy to hamper KRAS-induced tumorigenesis.
    Citation
    Shi L, Magee P, Fassan M, Sahoo S, Leong HS, Lee D, et al. A KRAS-responsive long non-coding RNA controls microRNA processing. Nat Commun. 2021;12(1):2038.
    Journal
    Nature Communications
    URI
    http://hdl.handle.net/10541/623956
    DOI
    10.1038/s41467-021-22337-3
    PubMed ID
    33795683
    Additional Links
    https://dx.doi.org/10.1038/s41467-021-22337-3
    Type
    Article
    Language
    en
    ae974a485f413a2113503eed53cd6c53
    10.1038/s41467-021-22337-3
    Scopus Count
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    All Paterson Institute for Cancer Research

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