STAT3-induced long noncoding RNAs in multiple myeloma cells display different properties in cancer

Abstract Interleukin-6 (IL-6)-activated Signal Transducer and Activator of Transcription 3 (STAT3) facilitates survival in the multiple myeloma cell line INA-6 and therefore represents an oncogenic key player. However, the biological mechanisms are still not fully understood. In previous studies we...

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Autores principales:	Stefanie Binder, Nadine Hösler, Diana Riedel, Ivonne Zipfel, Tilo Buschmann, Christoph Kämpf, Kristin Reiche, Renate Burger, Martin Gramatzki, Jörg Hackermüller, Peter F. Stadler, Friedemann Horn
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/b2635f07e4274b1dbd4f152516ba887d
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spelling	oai:doaj.org-article:b2635f07e4274b1dbd4f152516ba887d2021-12-02T12:32:07ZSTAT3-induced long noncoding RNAs in multiple myeloma cells display different properties in cancer10.1038/s41598-017-08348-52045-2322https://doaj.org/article/b2635f07e4274b1dbd4f152516ba887d2017-08-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-08348-5https://doaj.org/toc/2045-2322Abstract Interleukin-6 (IL-6)-activated Signal Transducer and Activator of Transcription 3 (STAT3) facilitates survival in the multiple myeloma cell line INA-6 and therefore represents an oncogenic key player. However, the biological mechanisms are still not fully understood. In previous studies we identified microRNA-21 as a STAT3 target gene with strong anti-apoptotic potential, suggesting that noncoding RNAs have an impact on the pathogenesis of human multiple myeloma. Here, we describe five long noncoding RNAs (lncRNAs) induced by IL-6-activated STAT3, which we named STAiRs. While STAiRs 1, 2 and 6 remain unprocessed in the nucleus and show myeloma-specific expression, STAiRs 15 and 18 are spliced and broadly expressed. Especially STAiR2 and STAiR18 are promising candidates. STAiR2 originates from the first intron of a tumor suppressor gene. Our data support a mutually exclusive expression of either STAiR2 or the functional tumor suppressor in INA-6 cells and thus a contribution of STAiR2 to tumorigenesis. Furthermore, STAiR18 was shown to be overexpressed in every tested tumor entity, indicating its global role in tumor pathogenesis. Taken together, our study reveals a number of STAT3-induced lncRNAs suggesting that the interplay between the coding and noncoding worlds represents a fundamental principle of STAT3-driven cancer development in multiple myeloma and beyond.Stefanie BinderNadine HöslerDiana RiedelIvonne ZipfelTilo BuschmannChristoph KämpfKristin ReicheRenate BurgerMartin GramatzkiJörg HackermüllerPeter F. StadlerFriedemann HornNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-13 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Stefanie Binder Nadine Hösler Diana Riedel Ivonne Zipfel Tilo Buschmann Christoph Kämpf Kristin Reiche Renate Burger Martin Gramatzki Jörg Hackermüller Peter F. Stadler Friedemann Horn STAT3-induced long noncoding RNAs in multiple myeloma cells display different properties in cancer
description	Abstract Interleukin-6 (IL-6)-activated Signal Transducer and Activator of Transcription 3 (STAT3) facilitates survival in the multiple myeloma cell line INA-6 and therefore represents an oncogenic key player. However, the biological mechanisms are still not fully understood. In previous studies we identified microRNA-21 as a STAT3 target gene with strong anti-apoptotic potential, suggesting that noncoding RNAs have an impact on the pathogenesis of human multiple myeloma. Here, we describe five long noncoding RNAs (lncRNAs) induced by IL-6-activated STAT3, which we named STAiRs. While STAiRs 1, 2 and 6 remain unprocessed in the nucleus and show myeloma-specific expression, STAiRs 15 and 18 are spliced and broadly expressed. Especially STAiR2 and STAiR18 are promising candidates. STAiR2 originates from the first intron of a tumor suppressor gene. Our data support a mutually exclusive expression of either STAiR2 or the functional tumor suppressor in INA-6 cells and thus a contribution of STAiR2 to tumorigenesis. Furthermore, STAiR18 was shown to be overexpressed in every tested tumor entity, indicating its global role in tumor pathogenesis. Taken together, our study reveals a number of STAT3-induced lncRNAs suggesting that the interplay between the coding and noncoding worlds represents a fundamental principle of STAT3-driven cancer development in multiple myeloma and beyond.
format	article
author	Stefanie Binder Nadine Hösler Diana Riedel Ivonne Zipfel Tilo Buschmann Christoph Kämpf Kristin Reiche Renate Burger Martin Gramatzki Jörg Hackermüller Peter F. Stadler Friedemann Horn
author_facet	Stefanie Binder Nadine Hösler Diana Riedel Ivonne Zipfel Tilo Buschmann Christoph Kämpf Kristin Reiche Renate Burger Martin Gramatzki Jörg Hackermüller Peter F. Stadler Friedemann Horn
author_sort	Stefanie Binder
title	STAT3-induced long noncoding RNAs in multiple myeloma cells display different properties in cancer
title_short	STAT3-induced long noncoding RNAs in multiple myeloma cells display different properties in cancer
title_full	STAT3-induced long noncoding RNAs in multiple myeloma cells display different properties in cancer
title_fullStr	STAT3-induced long noncoding RNAs in multiple myeloma cells display different properties in cancer
title_full_unstemmed	STAT3-induced long noncoding RNAs in multiple myeloma cells display different properties in cancer
title_sort	stat3-induced long noncoding rnas in multiple myeloma cells display different properties in cancer
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/b2635f07e4274b1dbd4f152516ba887d
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STAT3-induced long noncoding RNAs in multiple myeloma cells display different properties in cancer

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