Oncotarget

Research Papers:

miR-1238 inhibits cell proliferation by targeting LHX2 in non-small cell lung cancer

Xiangguang Shi, Lei Zhan, Can Xiao, Zhe Lei, Haiping Yang, Longqiang Wang, Jun Zhao and Hong-Tao Zhang _

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Oncotarget. 2015; 6:19043-19054. https://doi.org/10.18632/oncotarget.4232

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Abstract

Xiangguang Shi1,2,*, Lei Zhan1,2,*, Can Xiao3,*, Zhe Lei1,2, Haiping Yang1,2, Longqiang Wang1,2, Jun Zhao2,3 and Hong-Tao Zhang1,2

1 Soochow University Laboratory of Cancer Molecular Genetics, Medical College of Soochow University, Suzhou, China

2 Suzhou Key Laboratory for Molecular Cancer Genetics, Suzhou, China

3 The First Affiliated Hospital of Soochow University, Medical College of Soochow University, Suzhou, China

* These authors have contributed equally to this work

Correspondence to:

Hong-Tao Zhang, email:

Keywords: NSCLC, miR-1238, LHX2, cell proliferation

Received: January 30, 2015 Accepted: May 13, 2015 Published: May 22, 2015

Abstract

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.


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