转移是肺癌（LC）患者死亡的主要原因。 microRNA-611 (miR-611) 是一种 miRNA，在癌症中的研究很少。在此，我们的目的是进一步阐明miR-611在LC细胞中上皮间质转化（EMT）和转化生长因子-β（TGF-β）诱导的迁移中的作用及其可能的潜在机制。 miR-611 和 MAPKAP1 表达首先在转移性和非转移性患者的 LC 组织中发现，它们的表达与总生存期相关。进行功能获得和丧失实验以验证 miR-611 和 MAPKAP1 对 TGF-β 处理的 LC 细胞中 pAKT 表达、EMT 和迁移的影响。还通过荧光素酶报告基因测定确定了 miR-611 和 MAPKAP1 之间的相互作用。在我们的研究中，miR-611在LC组织中低水平表达，而MAPKAP1在LC组织中高表达，这与转移和短总生存期相关。从功能上来说，抑制 miR-611 或过表达 MAPKAP1 可加速 TGF-β 处理的 A549 和 H1299 细胞的 EMT 和迁移，并上调 pAKT。 miR-611 过表达或 MAPKAP1 沉默与 miR-611 抑制或 MAPKAP1 过表达产生相反的效果。从机制上讲，miR-611 可以靶向并下调 MAPKAP1。 LC 组织中 MAPKAP1 的表达也与 miR-611 的表达呈负相关。此外，miR-611过表达通过靶向MAPKAP1减少了TGF-β处理的A549和H1299细胞的EMT和迁移。总之，miR-611 过表达通过靶向 TGF-β 诱导的 LC 细胞中的 MAPKAP1 来减弱 EMT 和迁移，表明 miR-611 是 LC 治疗的生物靶点。版权所有 © 2024。由 Elsevier Inc. 出版。

Metastasis is a major cause of death in patients with lung cancer (LC). microRNA-611 (miR-611), a miRNA, has been little studied in cancer. Here, we aimed to further elucidate the roles of miR-611 in epithelial-mesenchymal transition (EMT) and migration induced by transforming growth factor-β (TGF-β) in LC cells and the possible underlying mechanisms. miR-611 and MAPKAP1 expression was first identified in LC tissues from metastatic and nonmetastatic patients, and their expression was associated with overall survival. Gain- and loss-of-function experiments were performed to verify the impacts of miR-611 and MAPKAP1 on pAKT expression, EMT, and migration in LC cells treated with TGF-β. The interaction between miR-611 and MAPKAP1 was also determined with a luciferase reporter assay. In our study, miR-611 was expressed at low levels, and MAPKAP1 was highly expressed in LC tissues, which was associated with metastasis and short overall survival. Functionally, miR-611 inhibition or MAPKAP1 overexpression accelerated EMT and migration and upregulated pAKT in TGF-β-treated A549 and H1299 cells; miR-611 overexpression or MAPKAP1 silencing exerted the opposite effects as miR-611 inhibition or MAPKAP1 overexpression. Mechanistically, miR-611 could target and downregulate MAPKAP1. MAPKAP1 expression was also negatively correlated with miR-611 expression in LC tissues. In addition, miR-611 overexpression reduced the EMT and migration of TGF-β-treated A549 and H1299 cells by targeting MAPKAP1. In conclusion, miR-611 overexpression attenuated EMT and migration by targeting MAPKAP1 in TGF-β-induced LC cells, indicating that miR-611 is a biological target for LC treatment.Copyright © 2024. Published by Elsevier Inc.