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miR‐30d is related to asbestos exposure and inhibits migration and invasion in NCI‐H2452 cells

机译:miR-30d与石棉暴露有关,并抑制NCI-H2452细胞中的迁移和侵袭

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摘要

Pleural malignant mesothelioma (MM) is a highly aggressive tumor that is typically related to asbestos exposure and has a latency of 20–60 years. Several microRNA contribute to MM initiation and progression, but the mechanisms are not clear. Here, we found that miR‐30d is downregulated in the pleural MM cell line NCI‐H2452, in the plasma of asbestos‐exposed individuals, and in asbestos‐exposed mesothelial cells. Furthermore, we investigated the influence of the overexpression of miR‐30d in pleural MM cells. We demonstrated that miR‐30d overexpression could suppress pleural MM cell proliferation, migration, and invasion in vitro and could promote cell apoptosis but could not significantly influence cell cycle. The mRNA and protein expression of vimentin and TWIST1 decreased, and the mRNA expression of CDH1 increased in NCI‐H2452 cells that overexpressed miR‐30d. We therefore conclude that miR‐30d is related to asbestos exposure and inhibits cell migration and invasion by regulating the epithelial–mesenchymal transition in NCI‐H2452 cells.
机译:胸膜恶性间皮瘤(MM)是一种高度侵袭性的肿瘤,通常与石棉暴露有关,潜伏期为20-60年。几种microRNA有助于MM的发生和发展,但机制尚不清楚。在这里,我们发现在胸膜MM细胞系NCI-H2452,接触石棉的个体血浆和接触石棉的间皮细胞中,miR-30d均下调。此外,我们研究了miR-30d在胸膜MM细胞中过表达的影响。我们证明了miR-30d的过表达可以在体外抑制胸膜MM细胞的增殖,迁移和侵袭,并且可以促进细胞凋亡,但不会显着影响细胞周期。在过度表达miR-30d的NCI-H2452细胞中,波形蛋白和TWIST1的mRNA和蛋白表达降低,而CDH1的mRNA表达升高。因此,我们得出结论,miR-30d与石棉暴露有关,并通过调节NCI-H2452细胞的上皮-间质转化来抑制细胞迁移和侵袭。

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