p53 induces formation of NEAT1 lncRNA-containing paraspeckles that modulate replication stress response and chemosensitivity View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2016-08

AUTHORS

Carmen Adriaens, Laura Standaert, Jasmine Barra, Mathilde Latil, Annelien Verfaillie, Peter Kalev, Bram Boeckx, Paul W G Wijnhoven, Enrico Radaelli, William Vermi, Eleonora Leucci, Gaëlle Lapouge, Benjamin Beck, Joost van den Oord, Shinichi Nakagawa, Tetsuro Hirose, Anna A Sablina, Diether Lambrechts, Stein Aerts, Cédric Blanpain, Jean-Christophe Marine

ABSTRACT

In a search for mediators of the p53 tumor suppressor pathway, which induces pleiotropic and often antagonistic cellular responses, we identified the long noncoding RNA (lncRNA) NEAT1. NEAT1 is an essential architectural component of paraspeckle nuclear bodies, whose pathophysiological relevance remains unclear. Activation of p53, pharmacologically or by oncogene-induced replication stress, stimulated the formation of paraspeckles in mouse and human cells. Silencing Neat1 expression in mice, which prevents paraspeckle formation, sensitized preneoplastic cells to DNA-damage-induced cell death and impaired skin tumorigenesis. We provide mechanistic evidence that NEAT1 promotes ATR signaling in response to replication stress and is thereby engaged in a negative feedback loop that attenuates oncogene-dependent activation of p53. NEAT1 targeting in established human cancer cell lines induced synthetic lethality with genotoxic chemotherapeutics, including PARP inhibitors, and nongenotoxic activation of p53. This study establishes a key genetic link between NEAT1 paraspeckles, p53 biology and tumorigenesis and identifies NEAT1 as a promising target to enhance sensitivity of cancer cells to both chemotherapy and p53 reactivation therapy. More... »

PAGES

861-868

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/nm.4135

    DOI

    http://dx.doi.org/10.1038/nm.4135

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1009076144

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/27376578


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