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    CKAP2L promotes non-small cell lung cancer progression through regulation of transcription elongation

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    Authors
    Monteverde, Tiziana
    Sahoo, Sudhakar
    La Montagna, Manuela
    Magee, Peter
    Shi, Lei
    Lee, David
    Sellers, Robert
    Baker, Alexander R
    Leong, Hui Sun
    Fassan, M.
    Garofalo, Michela
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    Affiliation
    CRUK MI, University of Manchester.
    Issue Date
    2021
    
    Metadata
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    Abstract
    Chromosomal instability (CIN) is a driver of clonal diversification and intra-tumor heterogeneity, providing genetic diversity that contributes to tumor progression. It is estimated that ∼80% of solid cancers, including non-small cell lung cancer (NSCLC), exhibit features of CIN, which affects tumor growth and response to therapy. However, the molecular mechanisms connecting CIN to tumor progression are still poorly understood. Through an RNAi screen performed on genes involved in CIN and overexpressed in human lung adenocarcinoma samples, we identified the cytoskeleton-associated protein 2-like (CKAP2L) as a potential oncogene that promotes lung cancer proliferation and growth in vitro and in vivo. Mechanistically, CKAP2L directly interacted with RNA Pol II and regulated transcription elongation of key genes involved in spindle assembly checkpoint, chromosome segregation, cell cycle, and E2F signaling. Furthermore, depletion of CKAP2L increased the sensitivity of NSCLC cells to alvocidib, a pan CDK inhibitor, leading to a significant reduction of cell proliferation and an increase in cell death. Altogether, these findings shed light on the molecular mechanisms through which CKAP2L, a protein involved in CIN, promotes cancer progression and suggest that its inhibition represents a novel therapeutic strategy in NSCLC.
    Citation
    Monteverde T, Sahoo S, La Montagna M, Magee P, Shi L, Lee D, et al. CKAP2L promotes non-small cell lung cancer progression through regulation of transcription elongation. Cancer Res. 2021.
    Journal
    Cancer Research
    URI
    http://hdl.handle.net/10541/623804
    DOI
    10.1158/0008-5472.Can-20-1968
    PubMed ID
    33472893
    Additional Links
    https://dx.doi.org/10.1158/0008-5472.Can-20-1968
    Type
    Article
    Language
    en
    ae974a485f413a2113503eed53cd6c53
    10.1158/0008-5472.Can-20-1968
    Scopus Count
    Collections
    All Paterson Institute for Cancer Research

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