Overexpression of LINC00152 correlates with poor patient survival and knockdown impairs cell proliferation in lung cancer

Abstract We employed RNA sequencing analysis to reveal dysregulated lncRNAs in lung cancer utilizing 461 lung adenocarcinomas and 156 normal lung tissues from 3 separate cohorts. We found that LINC00152 was highly overexpressed in lung tumors as compared to their adjacent normal tissues. Patients wi...

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Autores principales:	Shumei Feng, Jie Zhang, Wenmei Su, Shengbin Bai, Lei Xiao, Xiuyuan Chen, Jules Lin, Rishindra M. Reddy, Andrew C. Chang, David G. Beer, Guoan Chen
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/dcd1f9a01eb04543a30eb69b0cd9049a
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spelling	oai:doaj.org-article:dcd1f9a01eb04543a30eb69b0cd9049a2021-12-02T12:32:43ZOverexpression of LINC00152 correlates with poor patient survival and knockdown impairs cell proliferation in lung cancer10.1038/s41598-017-03043-x2045-2322https://doaj.org/article/dcd1f9a01eb04543a30eb69b0cd9049a2017-06-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-03043-xhttps://doaj.org/toc/2045-2322Abstract We employed RNA sequencing analysis to reveal dysregulated lncRNAs in lung cancer utilizing 461 lung adenocarcinomas and 156 normal lung tissues from 3 separate cohorts. We found that LINC00152 was highly overexpressed in lung tumors as compared to their adjacent normal tissues. Patients with high LINC00152 expression demonstrate a significantly poorer survival than those with low expression. We verified the diagnostic/prognostic potential of LINC00152 expression in an independent cohort of lung tumor tissues using quantitative RT-PCR. After knockdown of LINC00152 using siRNAs in lung cancer cell lines, both cell proliferation and colony formation were decreased. Cell fractionation and qRT-PCR analysis indicated that LINC00152 is found mainly in the cytoplasm. Treatment with Trichostatin A in cell lines having low LINC00152 expression indicated that histone acetylation may be one mechanism underlying LINC00152 overexpression in NSCLC. Western blot analyses indicated that p38a, STAT1, STAT3, CREB1, CCNE1 and c-MYC proteins were decreased after LINC00152 siRNA treatment. Our study indicates LINC00152 plays an important role in lung tumor growth and is potentially a diagnostic/prognostic marker. Further characterization of LINC00152 in regulating its target proteins may provide a novel therapeutic target of lung cancer.Shumei FengJie ZhangWenmei SuShengbin BaiLei XiaoXiuyuan ChenJules LinRishindra M. ReddyAndrew C. ChangDavid G. BeerGuoan ChenNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-10 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Shumei Feng Jie Zhang Wenmei Su Shengbin Bai Lei Xiao Xiuyuan Chen Jules Lin Rishindra M. Reddy Andrew C. Chang David G. Beer Guoan Chen Overexpression of LINC00152 correlates with poor patient survival and knockdown impairs cell proliferation in lung cancer
description	Abstract We employed RNA sequencing analysis to reveal dysregulated lncRNAs in lung cancer utilizing 461 lung adenocarcinomas and 156 normal lung tissues from 3 separate cohorts. We found that LINC00152 was highly overexpressed in lung tumors as compared to their adjacent normal tissues. Patients with high LINC00152 expression demonstrate a significantly poorer survival than those with low expression. We verified the diagnostic/prognostic potential of LINC00152 expression in an independent cohort of lung tumor tissues using quantitative RT-PCR. After knockdown of LINC00152 using siRNAs in lung cancer cell lines, both cell proliferation and colony formation were decreased. Cell fractionation and qRT-PCR analysis indicated that LINC00152 is found mainly in the cytoplasm. Treatment with Trichostatin A in cell lines having low LINC00152 expression indicated that histone acetylation may be one mechanism underlying LINC00152 overexpression in NSCLC. Western blot analyses indicated that p38a, STAT1, STAT3, CREB1, CCNE1 and c-MYC proteins were decreased after LINC00152 siRNA treatment. Our study indicates LINC00152 plays an important role in lung tumor growth and is potentially a diagnostic/prognostic marker. Further characterization of LINC00152 in regulating its target proteins may provide a novel therapeutic target of lung cancer.
format	article
author	Shumei Feng Jie Zhang Wenmei Su Shengbin Bai Lei Xiao Xiuyuan Chen Jules Lin Rishindra M. Reddy Andrew C. Chang David G. Beer Guoan Chen
author_facet	Shumei Feng Jie Zhang Wenmei Su Shengbin Bai Lei Xiao Xiuyuan Chen Jules Lin Rishindra M. Reddy Andrew C. Chang David G. Beer Guoan Chen
author_sort	Shumei Feng
title	Overexpression of LINC00152 correlates with poor patient survival and knockdown impairs cell proliferation in lung cancer
title_short	Overexpression of LINC00152 correlates with poor patient survival and knockdown impairs cell proliferation in lung cancer
title_full	Overexpression of LINC00152 correlates with poor patient survival and knockdown impairs cell proliferation in lung cancer
title_fullStr	Overexpression of LINC00152 correlates with poor patient survival and knockdown impairs cell proliferation in lung cancer
title_full_unstemmed	Overexpression of LINC00152 correlates with poor patient survival and knockdown impairs cell proliferation in lung cancer
title_sort	overexpression of linc00152 correlates with poor patient survival and knockdown impairs cell proliferation in lung cancer
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/dcd1f9a01eb04543a30eb69b0cd9049a
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Overexpression of LINC00152 correlates with poor patient survival and knockdown impairs cell proliferation in lung cancer

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