期刊
ONCOTARGET
卷 6, 期 22, 页码 19043-19054出版社
IMPACT JOURNALS LLC
DOI: 10.18632/oncotarget.4232
关键词
NSCLC; miR-1238; LHX2; cell proliferation
资金
- National Natural Science Foundation of China [81372277, 81171894]
- Jiangsu Province's Key Provincial Talents Program [RC2011106]
- Science and Technology Committee of Jiangsu Province [BK20131159]
- 333 Project of Jiangsu Province Government
- Jiangsu Provincial Department of Education [14KJB310017, CXZZ13_0830]
- Soochow Scholar Project of Soochow University [SDR201051]
- Suzhou Key Laboratory for Molecular Cancer Genetics [SZS201209]
- Priority Academic Program Development of Jiangsu Higher Education Institutions (PAPD)
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-alpha-2 cells inhibited endogenous expression of LHX2 mRNA and protein. Moreover, ectopic expression of miR-1238 in NSCLC A549 and LTEP-alpha-2 cells suppressed cellular viability and proliferation. siRNA-induced knockdown of LHX2 copied the phenotype of miR-1238 overexpression in NSCLC A549 and LTEP-alpha-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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