MicroRNA-212 suppresses nonsmall lung cancer invasion and migration by regulating ubiquitin-specific protease-9
MicroRNA-212 suppresses nonsmall lung cancer invasion and migration by regulating ubiquitin-specific protease-9
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MicroRNA-212通过调节泛素特异性蛋白酶9抑制非小细胞肺癌侵袭和迁移
DOI：
10.1002/jcb.27939
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发表时间：
2019-04-01
影响因子：
4
通讯作者：
Chai, Kequn
中科院分区：
文献类型：
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作者：
Chen, Wei;Huang, Yuye;Chai, Kequn
MicroRNAs （miRNAs）在迁移、增殖、分化、细胞周期和细胞凋亡等多种生物过程中发挥着至关重要的作用。在许多肿瘤细胞中，上皮-间质转化（Epithelial-mesenchymal transition， EMT）已被证明与迁移和侵袭能力有关。在这项研究中，我们分别用伤口愈合试验和跨井侵袭来分析非小细胞肺癌（NSCLC）的迁移和侵袭能力。实时定量聚合酶链反应检测泛素特异性蛋白酶-9- x -linked （USP9X）和miR-212信使RNA （mRNA）的表达，Western blot检测E-cadherin和vimentin的表达。我们的研究结果表明，miR-212模拟物抑制细胞迁移和侵袭，而miR-212抑制剂增加细胞迁移和侵袭。WP1130组与miR-212 mimic联合WP1130组之间无显著差异。此外，WP1130抑制了NSCLC细胞的迁移和侵袭能力。Western blot分析显示，miR-212模拟E-cadherin表达上调和vimentin表达下调，而miR-212抑制剂下调E-cadherin表达上调vimentin表达。这些数据表明，miR-212通过调节USP9X的表达来调节NSCLC细胞的侵袭和迁移。综上所述，这些发现表明miR-212通过靶向参与EMT的USP9X调控NSCLC细胞的迁移和侵袭。
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.