MicroRNA-200c inhibits the metastasis of non-small cell lung cancer cells by targeting ZEB2, an epithelial-mesenchymal transition regulator (Retracted article. See vol. 24, pg. 573, 2021)
MicroRNA-200c inhibits the metastasis of non-small cell lung cancer cells by targeting ZEB2, an epithelial-mesenchymal transition regulator (Retracted article. See vol. 24, pg. 573, 2021)
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DOI：
10.3892/mmr.2016.4901
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发表时间：
2016-04-01
影响因子：
3.4
通讯作者：
Li, Junxia
中科院分区：
文献类型：
--
作者：
Jiao, Aihong;Sui, Minghua;Li, Junxia
MicroRNAs （miRs）已被证明可以调节人类癌症的各种生物过程，包括非小细胞肺癌（NSCLC）。然而，关于miR-200c在介导NSCLC恶性进展中的确切作用及其潜在机制的证据很少。本研究旨在探讨miR-200c在非小细胞肺癌进展中的作用。通过逆转录-定量聚合酶链反应测定，与正常肺上皮细胞相比，miR-200c在NSCLC细胞系中的表达水平显著降低。过表达miR-200c可显著抑制A549 NSCLC细胞的迁移和侵袭。荧光素酶报告基因试验的结果进一步确定锌指E-box-binding homeobox 2 （ZEB2）是miR-200c的直接靶基因，并且在过表达miR-200c的A549细胞中，ZEB2的表达被抑制。此外，小干扰rna介导的ZEB2抑制抑制了A549细胞的迁移和侵袭。此外，由于ZEB2是上皮-间充质转化（EMT）调节剂，我们进一步研究了miR-200c在NSCLC细胞EMT调控中的作用。western blot分析结果显示，过表达miR-200c可上调A549细胞中E-cadherin的表达，下调N-cadherin和vimentin的表达，表明EMT受到抑制。基于这些结果，本研究提示miR-200c能够通过靶向ZEB2抑制NSCLC细胞的转移。因此，miR-200c可能被认为是治疗NSCLC的潜在候选者。
MicroRNAs (miRs) have been demonstrated to regulate various biological processes in human cancer, including non-small cell lung cancer (NSCLC). However, little evidence has been provided regarding the exact role of miR-200c in mediating the malignant progression of NSCLC, as well as the underlying mechanism. The present study aimed to investigate the putative role of miR-200c in the progression of NSCLC. The expression levels of miR-200c were significantly reduced in NSCLC cell lines compared with in normal lung epithelial cells, as determined by reverse transcription-quantitative polymerase chain reaction. Overexpression of miR-200c significantly suppressed cell migration and invasion of A549 NSCLC cells. Results of a luciferase reporter assay further identified zinc finger E-box-binding homeobox 2 (ZEB2) as a direct target gene of miR-200c, and the expression of ZEB2 was shown to be suppressed in A549 cells overexpressing miR-200c. Furthermore, small interfering RNA-mediated inhibition of ZEB2 suppressed the migration and invasion of A549 cells. In addition, since ZEB2 is an epithelial-mesenchymal transition (EMT) regulator, the role of miR-200c in the regulation of EMT in NSCLC cells was further examined. Results of a western blot analysis indicated that overexpression of miR-200c upregulated E-cadherin, and downregulated N-cadherin and vimentin expression in A549 cells, thus suggesting that EMT was suppressed. Based on these results, the present study suggested that miR-200c was able to inhibit the metastasis of NSCLC cells by targeting ZEB2. Therefore, miR-200c may be considered as a potential candidate for the treatment of NSCLC.