Loss of the abundant nuclear non-coding RNA MALAT1 is compatible with life and development
The metastasis-associated lung adenocarcinoma transcript 1, MALAT1, is a long non-coding RNA (lncRNA) that has been discovered as a marker for lung cancer metastasis. It is highly abundant, its expression is strongly regulated in many tumor entities including lung adenocarcinoma and hepatocellular c...
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| Hauptverfasser: | , , , , , |
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| Dokumenttyp: | Article (Journal) |
| Sprache: | Englisch |
| Veröffentlicht: |
1 August 2012
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| In: |
RNA biology
Year: 2012, Jahrgang: 9, Heft: 8, Pages: 1076-1087 |
| ISSN: | 1555-8584 |
| DOI: | 10.4161/rna.21089 |
| Online-Zugang: | Verlag, Volltext: http://dx.doi.org/10.4161/rna.21089 Verlag, Volltext: https://doi.org/10.4161/rna.21089 
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| Verfasserangaben: | Moritz Eißmann, Tony Gutschner, Monika Hämmerle, Stefan Günther, Maïwen Caudron-Herger, Matthias Groß, Peter Schirmacher, Karsten Rippe, Thomas Braun, Martin Zörnig and Sven Diederichs |
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| 245 | 1 | 0 | |a Loss of the abundant nuclear non-coding RNA MALAT1 is compatible with life and development |c Moritz Eißmann, Tony Gutschner, Monika Hämmerle, Stefan Günther, Maïwen Caudron-Herger, Matthias Groß, Peter Schirmacher, Karsten Rippe, Thomas Braun, Martin Zörnig and Sven Diederichs |
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| 520 | |a The metastasis-associated lung adenocarcinoma transcript 1, MALAT1, is a long non-coding RNA (lncRNA) that has been discovered as a marker for lung cancer metastasis. It is highly abundant, its expression is strongly regulated in many tumor entities including lung adenocarcinoma and hepatocellular carcinoma as well as physiological processes, and it is associated with many RNA binding proteins and highly conserved throughout evolution. The nuclear transcript MALAT-1 has been functionally associated with gene regulation and alternative splicing and its regulation has been shown to impact proliferation, apoptosis, migration and invasion. Here, we have developed a human and a mouse knockout system to study the loss-of-function phenotypes of this important ncRNA. In human tumor cells, MALAT1 expression was abrogated using Zinc Finger Nucleases. Unexpectedly, the quantitative loss of MALAT1 did neither affect proliferation nor cell cycle progression nor nuclear architecture in human lung or liver cancer cells. Moreover, genetic loss of Malat1 in a knockout mouse model did not give rise to any obvious phenotype or histological abnormalities in Malat1-null compared with wild-type animals. Thus, loss of the abundant nuclear long ncRNA MALAT1 is compatible with cell viability and normal development. | ||
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