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

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 L...

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Autores principales: Feng, Shumei, Zhang, Jie, Su, Wenmei, Bai, Shengbin, Xiao, Lei, Chen, Xiuyuan, Lin, Jules, Reddy, Rishindra M., Chang, Andrew C., Beer, David G., Chen, Guoan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5462773/
https://www.ncbi.nlm.nih.gov/pubmed/28592840
http://dx.doi.org/10.1038/s41598-017-03043-x
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author Feng, Shumei
Zhang, Jie
Su, Wenmei
Bai, Shengbin
Xiao, Lei
Chen, Xiuyuan
Lin, Jules
Reddy, Rishindra M.
Chang, Andrew C.
Beer, David G.
Chen, Guoan
author_facet Feng, Shumei
Zhang, Jie
Su, Wenmei
Bai, Shengbin
Xiao, Lei
Chen, Xiuyuan
Lin, Jules
Reddy, Rishindra M.
Chang, Andrew C.
Beer, David G.
Chen, Guoan
author_sort Feng, Shumei
collection PubMed
description 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.
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spelling pubmed-54627732017-06-08 Overexpression of LINC00152 correlates with poor patient survival and knockdown impairs cell proliferation in lung cancer Feng, Shumei Zhang, Jie Su, Wenmei Bai, Shengbin Xiao, Lei Chen, Xiuyuan Lin, Jules Reddy, Rishindra M. Chang, Andrew C. Beer, David G. Chen, Guoan Sci Rep Article 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. Nature Publishing Group UK 2017-06-07 /pmc/articles/PMC5462773/ /pubmed/28592840 http://dx.doi.org/10.1038/s41598-017-03043-x Text en © The Author(s) 2017 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
spellingShingle Article
Feng, Shumei
Zhang, Jie
Su, Wenmei
Bai, Shengbin
Xiao, Lei
Chen, Xiuyuan
Lin, Jules
Reddy, Rishindra M.
Chang, Andrew C.
Beer, David G.
Chen, Guoan
Overexpression of LINC00152 correlates with poor patient survival and knockdown impairs cell proliferation in lung cancer
title 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_short 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
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5462773/
https://www.ncbi.nlm.nih.gov/pubmed/28592840
http://dx.doi.org/10.1038/s41598-017-03043-x
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