SNHG5 promotes colorectal cancer cell survival by counteracting STAU1-mediated mRNA destabilization

Nkerorema Djodji Damas, Michela Marcatti, Christophe Côme, Lise Lotte Christensen, Morten Muhlig Nielsen, Roland Baumgartner, Helene Maria Gylling, Giulia Maglieri, Carsten Friis Rundsten, Stefan E. Seemann, Nicolas Rapin, Simon Thézenas, Søren Vang, Torben Ørntoft, Claus Lindbjerg Andersen, Jakob Skou Pedersen and Anders H. Lund ()
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Nkerorema Djodji Damas: Biotech Research and Innovation Centre, University of Copenhagen
Michela Marcatti: Biotech Research and Innovation Centre, University of Copenhagen
Christophe Côme: Biotech Research and Innovation Centre, University of Copenhagen
Lise Lotte Christensen: Aarhus University Hospital
Morten Muhlig Nielsen: Aarhus University Hospital
Roland Baumgartner: Biotech Research and Innovation Centre, University of Copenhagen
Helene Maria Gylling: Biotech Research and Innovation Centre, University of Copenhagen
Giulia Maglieri: Biotech Research and Innovation Centre, University of Copenhagen
Carsten Friis Rundsten: Biotech Research and Innovation Centre, University of Copenhagen
Stefan E. Seemann: Center for Non-Coding RNA in Technology and Health, University of Copenhagen
Nicolas Rapin: Biotech Research and Innovation Centre, University of Copenhagen
Simon Thézenas: Biostatistics Unit, Institut Régional du Cancer de Montpellier (ICM)—Val d’Aurelle
Søren Vang: Aarhus University Hospital
Torben Ørntoft: Aarhus University Hospital
Claus Lindbjerg Andersen: Aarhus University Hospital
Jakob Skou Pedersen: Aarhus University Hospital
Anders H. Lund: Biotech Research and Innovation Centre, University of Copenhagen

Nature Communications, 2016, vol. 7, issue 1, 1-14

Abstract: Abstract We currently have limited knowledge of the involvement of long non-coding RNAs (lncRNAs) in normal cellular processes and pathologies. Here, we identify and characterize SNHG5 as a stable cytoplasmic lncRNA with up-regulated expression in colorectal cancer. Depletion of SNHG5 induces cell cycle arrest and apoptosis in vitro and limits tumour outgrowth in vivo, whereas SNHG5 overexpression counteracts oxaliplatin-induced apoptosis. Using an unbiased approach, we identify 121 transcript sites interacting with SNHG5 in the cytoplasm. Importantly, knockdown of key SNHG5 target transcripts, including SPATS2, induces apoptosis and thus mimics the effect seen following SNHG5 depletion. Mechanistically, we suggest that SNHG5 stabilizes the target transcripts by blocking their degradation by STAU1. Accordingly, depletion of STAU1 rescues the apoptosis induced after SNHG5 knockdown. Hence, we characterize SNHG5 as a lncRNA promoting tumour cell survival in colorectal cancer and delineate a novel mechanism in which a cytoplasmic lncRNA functions through blocking the action of STAU1.

Date: 2016
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DOI: 10.1038/ncomms13875

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