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Targeting LINC00673 expression triggers cellular senescence in lung cancer

Aberrant expression of noncoding RNAs plays a critical role during tumorigenesis. To uncover novel functions of long non-coding RNA (lncRNA) in lung adenocarcinoma, we used a microarray-based screen identifying LINC00673 with elevated expression in matched tumor versus normal tissue. We report that...

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Main Authors: Roth, Anna (Author) , Warth, Arne (Author) , Schnabel, Philipp Albert (Author) , Muley, Thomas (Author) , Meister, Michael (Author) , Zabeck, Heike (Author) , Hoffmann, Hans (Author)
Format: Article (Journal)
Language:English
Published: 7 December 2018
In: RNA biology
Year: 2018, Volume: 15, Issue: 12, Pages: 1499-1511
ISSN:1555-8584
DOI:10.1080/15476286.2018.1553481
Online Access:Verlag, Volltext: https://doi.org/10.1080/15476286.2018.1553481
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Author Notes:Anna Roth, Karine Boulay, Matthias Groß, Maria Polycarpou-Schwarz, Frédérick A. Mallette, Marine Regnier, Or Bida, Doron Ginsberg, Arne Warth, Philipp A. Schnabel, Thomas Muley, Michael Meister, Heike Zabeck, Hans Hoffmann & Sven Diederichs

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520 |a Aberrant expression of noncoding RNAs plays a critical role during tumorigenesis. To uncover novel functions of long non-coding RNA (lncRNA) in lung adenocarcinoma, we used a microarray-based screen identifying LINC00673 with elevated expression in matched tumor versus normal tissue. We report that loss of LINC00673 is sufficient to trigger cellular senescence, a tumor suppressive mechanism associated with permanent cell cycle arrest, both in lung cancer and normal cells in a p53-dependent manner. LINC00673-depleted cells fail to efficiently transit from G1- to S-phase. Using a quantitative proteomics approach, we confirm the modulation of senescence-associated genes as a result of LINC00673 knockdown. In addition, we uncover that depletion of p53 in normal and tumor cells is sufficient to overcome LINC00673-mediated cell cycle arrest and cellular senescence. Furthermore, we report that overexpression of LINC00673 reduces p53 translation and contributes to the bypass of Ras-induced senescence. In summary, our findings highlight LINC00673 as a crucial regulator of proliferation and cellular senescence in lung cancer. 
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