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miR‐497‐5p inhibits tumor cell growth and invasion by targeting SOX5 in non–small‐cell lung cancer
Author(s) -
Li Gang,
Wang Kai,
Wang Jiansheng,
Qin Sida,
Sun Xin,
Ren Hong
Publication year - 2019
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.28345
Subject(s) - cell growth , microrna , downregulation and upregulation , a549 cell , apoptosis , cancer research , cell , lung cancer , cell migration , cell culture , biology , microbiology and biotechnology , chemistry , gene , medicine , genetics
MicroRNAs plays an important role in the ccurrence and development of non–small‐cell lung cancer (NSCLC). miR‐497‐5p has been reported to function as a tumor suppressor in various cancers. However, the role of miR‐497‐5p in NSCLC remains poorly understood. In this study, we aimed to investigate the biological role and potential molecular mechanism of miR‐497‐5p in NSCLC. Our results showed that the messenger RNA (mRNA) expression level of miR‐497‐5p was notably downregulated in human NSCLC tissues and cell lines. miR‐497‐5p overexpression remarkably inhibited NSCLC cell proliferation and increased cell apoptosis in A549 and H460 cells, whereas inhibition of miR‐497‐5p had an opposite effect. The ability of cell migration and invasion was inhibited by miR‐497‐5p overexpression but was increased by miR‐497‐5p inhibition. Moreover, our findings indicated that SOX5 was a direct target of miR‐497‐5p. The protein and mRNA expression levels of SOX5 in A549 cells were remarkably inhibited by miR‐497‐5p overexpression but was upregulated by miR‐497‐5p inhibition. Furthermore, SOX5 overexpression notably reversed the effect of miR‐497‐5p mimic on NSCLC cell proliferation, cell apoptosis, cell migration, and invasion. Taken together, these results indicated that miR‐497‐5p overexpression inhibited NSCLC cell proliferation, migration and invasion, and induced cell apoptosis through inhibiting SOX5 gene expression. It was conceivable that miR‐497‐5p might serve as a potential molecular target for NSCLC treatment.