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miR-1238 inhibits cell proliferation by targeting LHX2 in non-small cell lung cancer
In human cancers, dysregulated expression of LIM-homeobox gene 2 (LHX2) and downregulation of miR-1238 has been reported separately. However, the relationship between them remains unclear. We investigated the functional contribution of miR-1238 to the regulation of LHX2 in non-small cell lung cancer...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Impact Journals LLC
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4662474/ https://www.ncbi.nlm.nih.gov/pubmed/26189214 |
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author | Shi, Xiangguang Zhan, Lei Xiao, Can Lei, Zhe Yang, Haiping Wang, Longqiang Zhao, Jun Zhang, Hong-Tao |
author_facet | Shi, Xiangguang Zhan, Lei Xiao, Can Lei, Zhe Yang, Haiping Wang, Longqiang Zhao, Jun Zhang, Hong-Tao |
author_sort | Shi, Xiangguang |
collection | PubMed |
description | In human cancers, dysregulated expression of LIM-homeobox gene 2 (LHX2) and downregulation of miR-1238 has been reported separately. However, the relationship between them remains unclear. We investigated the functional contribution of miR-1238 to the regulation of LHX2 in non-small cell lung cancer (NSCLC). Here, computational algorithms predicted that the 3′-untranslated region (3′-UTR) of LHX2 is a target of miR-1238. Luciferase assays validated that miR-1238 directly bound to 3′-UTR of LHX2. qRT-PCR and western blot analyses further confirmed that overexpression of miR-1238 mimic in NSCLC A549 and LTEP-α-2 cells inhibited endogenous expression of LHX2 mRNA and protein. Moreover, ectopic expression of miR-1238 in NSCLC A549 and LTEP-α-2 cells suppressed cellular viability and proliferation. siRNA-induced knockdown of LHX2 copied the phenotype of miR-1238 overexpression in NSCLC A549 and LTEP-α-2 cells and LHX2 knockdown inhibited cell cycle. In addition, miR-1238 expression was frequently decreased in human NSCLC tissues and reversely correlated with LHX2 expression, which was increased in NSCLC tissues. Collectively, our findings demonstrate that miR-1238 inhibit the proliferation of NSCLC cells at least partly via repression of LHX2, shedding light on the mechanistic interaction of miR-1238 and LHX2 in NSCLC carcinogenesis. Furthermore, our data suggest that expression of miR-1238 could be a promising therapeutic strategy for NSCLC treatment. |
format | Online Article Text |
id | pubmed-4662474 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | Impact Journals LLC |
record_format | MEDLINE/PubMed |
spelling | pubmed-46624742015-12-02 miR-1238 inhibits cell proliferation by targeting LHX2 in non-small cell lung cancer Shi, Xiangguang Zhan, Lei Xiao, Can Lei, Zhe Yang, Haiping Wang, Longqiang Zhao, Jun Zhang, Hong-Tao Oncotarget Research Paper In human cancers, dysregulated expression of LIM-homeobox gene 2 (LHX2) and downregulation of miR-1238 has been reported separately. However, the relationship between them remains unclear. We investigated the functional contribution of miR-1238 to the regulation of LHX2 in non-small cell lung cancer (NSCLC). Here, computational algorithms predicted that the 3′-untranslated region (3′-UTR) of LHX2 is a target of miR-1238. Luciferase assays validated that miR-1238 directly bound to 3′-UTR of LHX2. qRT-PCR and western blot analyses further confirmed that overexpression of miR-1238 mimic in NSCLC A549 and LTEP-α-2 cells inhibited endogenous expression of LHX2 mRNA and protein. Moreover, ectopic expression of miR-1238 in NSCLC A549 and LTEP-α-2 cells suppressed cellular viability and proliferation. siRNA-induced knockdown of LHX2 copied the phenotype of miR-1238 overexpression in NSCLC A549 and LTEP-α-2 cells and LHX2 knockdown inhibited cell cycle. In addition, miR-1238 expression was frequently decreased in human NSCLC tissues and reversely correlated with LHX2 expression, which was increased in NSCLC tissues. Collectively, our findings demonstrate that miR-1238 inhibit the proliferation of NSCLC cells at least partly via repression of LHX2, shedding light on the mechanistic interaction of miR-1238 and LHX2 in NSCLC carcinogenesis. Furthermore, our data suggest that expression of miR-1238 could be a promising therapeutic strategy for NSCLC treatment. Impact Journals LLC 2015-05-22 /pmc/articles/PMC4662474/ /pubmed/26189214 Text en Copyright: © 2015 Shi et al. http://creativecommons.org/licenses/by/2.5/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. |
spellingShingle | Research Paper Shi, Xiangguang Zhan, Lei Xiao, Can Lei, Zhe Yang, Haiping Wang, Longqiang Zhao, Jun Zhang, Hong-Tao miR-1238 inhibits cell proliferation by targeting LHX2 in non-small cell lung cancer |
title | miR-1238 inhibits cell proliferation by targeting LHX2 in non-small cell lung cancer |
title_full | miR-1238 inhibits cell proliferation by targeting LHX2 in non-small cell lung cancer |
title_fullStr | miR-1238 inhibits cell proliferation by targeting LHX2 in non-small cell lung cancer |
title_full_unstemmed | miR-1238 inhibits cell proliferation by targeting LHX2 in non-small cell lung cancer |
title_short | miR-1238 inhibits cell proliferation by targeting LHX2 in non-small cell lung cancer |
title_sort | mir-1238 inhibits cell proliferation by targeting lhx2 in non-small cell lung cancer |
topic | Research Paper |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4662474/ https://www.ncbi.nlm.nih.gov/pubmed/26189214 |
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