Therapeutic targeting of the PLK1-PRC1-axis triggers cell death in genomically silent childhood cancer View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2021-09-16

AUTHORS

Jing Li, Shunya Ohmura, Aruna Marchetto, Martin F. Orth, Roland Imle, Marlene Dallmayer, Julian Musa, Maximilian M. L. Knott, Tilman L. B. Hölting, Stefanie Stein, Cornelius M. Funk, Ana Sastre, Javier Alonso, Felix Bestvater, Merve Kasan, Laura Romero-Pérez, Wolfgang Hartmann, Andreas Ranft, Ana Banito, Uta Dirksen, Thomas Kirchner, Florencia Cidre-Aranaz, Thomas G. P. Grünewald

ABSTRACT

Chromosomal instability (CIN) is a hallmark of cancer1. Yet, many childhood cancers, such as Ewing sarcoma (EwS), feature remarkably ‘silent’ genomes with minimal CIN2. Here, we show in the EwS model how uncoupling of mitosis and cytokinesis via targeting protein regulator of cytokinesis 1 (PRC1) or its activating polo-like kinase 1 (PLK1) can be employed to induce fatal genomic instability and tumor regression. We find that the EwS-specific oncogenic transcription factor EWSR1-FLI1 hijacks PRC1, which physiologically safeguards controlled cell division, through binding to a proximal enhancer-like GGAA-microsatellite, thereby promoting tumor growth and poor clinical outcome. Via integration of transcriptome-profiling and functional in vitro and in vivo experiments including CRISPR-mediated enhancer editing, we discover that high PRC1 expression creates a therapeutic vulnerability toward PLK1 inhibition that can repress even chemo-resistant EwS cells by triggering mitotic catastrophe.Collectively, our results exemplify how aberrant PRC1 activation by a dominant oncogene can confer malignancy but provide opportunities for targeted therapy, and identify PRC1 expression as an important determinant to predict the efficacy of PLK1 inhibitors being used in clinical trials. More... »

PAGES

5356

References to SciGraph publications

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  • Journal

    TITLE

    Nature Communications

    ISSUE

    1

    VOLUME

    12

    Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/s41467-021-25553-z

    DOI

    http://dx.doi.org/10.1038/s41467-021-25553-z

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1141149343

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/34531368


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