This study aimed to investigate the mechanism of miR-142-5p and Yin Yang 1 (YY1) on regulating epithelial–mesenchymal transition (EMT) in lung cancer cell metastasis. The expressions of YY1 and miR-142-5p in different lung cancer cell lines were negatively correlated. The results of the dual-luciferase reporter assay further validated that miR-142-5p directly targeted YY1. Subsequently, transwell assays, wound-healing assay, and transplantation tumor model in nude mice proved that YY1 could promote the metastasis of lung cancer cells, whereas miR-142-5p impaired the stimulating effect of YY1 on the metastasis ability of lung cancer cells in vitro and in vivo. Western blot and quantitative real-time polymerase chain reaction analysis of the EMT-related proteins indicated that YY1 could enhance the metastasis ability of lung cancer cells by promoting EMT. On the contrary, miR-142-5p constrained the expression of mesenchymal markers by targeting YY1, reversed the differentiation of cells into mesenchymal cells, and weakened the metastasis ability of tumor cells in vitro and in vivo. In summary, miR-142-5p may regulate the expressions of EMT-related proteins by targeting YY1, thereby inhibiting lung cancer metastasis, which provides a promising therapeutic target for lung cancer.

中文翻译：

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MiR-142-5p 通过靶向阴阳 1 来抑制肺癌细胞转移以调节上皮-间质转化

本研究旨在探讨miR-142-5p和Yin Yang 1 (YY1)在肺癌细胞转移中调节上皮-间质转化(EMT)的机制。YY1和miR-142-5p在不同肺癌细胞系中的表达呈负相关。双荧光素酶报告基因检测的结果进一步验证了 miR-142-5p 直接靶向 YY1。随后，transwell 试验、伤口愈合试验和裸鼠移植肿瘤模型证明 YY1 可以促进肺癌细胞的转移，而 miR-142-5p 会削弱 YY1 对肺癌细胞转移能力的刺激作用。体外和体内. EMT相关蛋白的Western印迹和定量实时聚合酶链反应分析表明，YY1可通过促进EMT增强肺癌细胞的转移能力。相反，miR-142-5p通过靶向YY1来限制间充质标志物的表达，逆转细胞向间充质细胞的分化，削弱肿瘤细胞在体内外的转移能力。综上所述，miR-142-5p可能通过靶向YY1调控EMT相关蛋白的表达，从而抑制肺癌转移，为肺癌的治疗提供了一个有希望的靶点。