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MicroRNA‐212 suppresses nonsmall lung cancer invasion and migration by regulating ubiquitin‐specific protease‐9
Author(s) -
Chen Wei,
Huang Yuye,
Zhang Shufen,
Zheng Xiaoxiao,
Xie Shangzhi,
Mao Jiayan,
Cai Ying,
Lu Xuemei,
Hu Liqiang,
Shen Jian,
Dong Ying,
Chai Kequn
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.27939
Subject(s) - vimentin , cell migration , epithelial–mesenchymal transition , microrna , downregulation and upregulation , western blot , cancer research , biology , small interfering rna , cell growth , cell , gentamicin protection assay , apoptosis , ubiquitin , microbiology and biotechnology , cell culture , transfection , immunology , immunohistochemistry , gene , biochemistry , genetics
MicroRNAs (miRNAs) play crucial roles in various biological processes, including migration, proliferation, differentiation, cell cycling, and apoptosis. Epithelial‐mesenchymal transition (EMT) has been shown to be related to the capability of migration and invasion in many tumor cells. In this study, we used wound‐healing assay and transwell invasion to analysis the capability of migration and invasion in non–small‐cell lung carcinoma (NSCLC), respectively. The expression of ubiquitin‐specific protease‐9‐X‐linked (USP9X) and miR‐212 messenger RNA (mRNA) was determined by quantitative real‐time polymerase chain reaction and Western blot analysis was used to determine the E‐cadherin and vimentin expression. Our results showed that miR‐212 mimic inhibited cell migration and invasion, while miR‐212 inhibitor increased cell migration and invasion. There was no significant difference between WP1130 and miR‐212 mimic combined with WP1130 groups. Moreover, WP1130 inhibited the capability of the migration and invasion of NSCLC cells. Western blot analysis displayed that miR‐212 mimic upregulated E‐cadherin expression and downregulated vimentin expression, while miR‐212 inhibitor downregulated E‐cadherin and upregulated vimentin expression. These data showed that miR‐212 regulated NSCLC cell invasion and migration by regulating USP9X expression. Taken together, these findings indicated that miR‐212 regulated NSCLC cells migration and invasion through targeting USP9X involved in EMT.