SMARCE1 suppresses EGFR expression and controls responses to MET and ALK inhibitors in lung cancer View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2015-04

AUTHORS

Andreas I Papadakis, Chong Sun, Theo A Knijnenburg, Yibo Xue, Wipawadee Grernrum, Michael Hölzel, Wouter Nijkamp, Lodewyk FA Wessels, Roderick L Beijersbergen, Rene Bernards, Sidong Huang

ABSTRACT

Recurrent inactivating mutations in components of SWI/SNF chromatin-remodeling complexes have been identified across cancer types, supporting their roles as tumor suppressors in modulating oncogenic signaling pathways. We report here that SMARCE1 loss induces EGFR expression and confers resistance to MET and ALK inhibitors in non-small cell lung cancers (NSCLCs). We found that SMARCE1 binds to regulatory regions of the EGFR locus and suppresses EGFR transcription in part through regulating expression of Polycomb Repressive Complex component CBX2. Addition of the EGFR inhibitor gefitinib restores the sensitivity of SMARCE1-knockdown cells to MET and ALK inhibitors in NSCLCs. Our findings link SMARCE1 to EGFR oncogenic signaling and suggest targeted treatment options for SMARCE1-deficient tumors. More... »

PAGES

445

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/cr.2015.16

    DOI

    http://dx.doi.org/10.1038/cr.2015.16

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1033720446

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/25656847


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