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Low miR-145 silenced by DNA methylation promotes NSCLC cell proliferation migration and invasion by targeting mucin 1

机译:DNA甲基化沉默的低miR-145通过靶向粘蛋白1促进NSCLC细胞增殖迁移和侵袭

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摘要

MiR-145 has been implicated in the progression of non-small cell lung cancer (NSCLC); however, its exact mechanism is not well established. Here, we report that miR-145 expression is decreased in NSCLC cell lines and tumor tissues and that this low level of expression is associated with DNA methylation. MiR-145 methylation in NSCLC was correlated with a more aggressive tumor phenotype and was associated with poor survival time, as shown by Kaplan-Meier analysis. Additional multivariate Cox regression analysis indicated that miR-145 methylation was an independent prognostic factor for poor survival in patients with NSCLC. Furthermore, we found that restoration of miR-145 expression inhibited proliferation, migration and invasion of NSCLC by the direct targeting of mucin 1 by miR-145. Our results indicate that low miR-145 expression, due to methylation, promotes NSCLC cell proliferation, migration and invasion by targeting mucin 1. Therefore, miR-145 may be a valuable therapeutic target for NSCLC.
机译:MiR-145与非小细胞肺癌(NSCLC)的发展有关。但是,其确切机制尚不完善。在这里,我们报道在NSCLC细胞系和肿瘤组织中miR-145的表达降低,而这种低水平的表达与DNA甲基化有关。如Kaplan-Meier分析所示,NSCLC中的MiR-145甲基化与更具侵略性的肿瘤表型相关,并且与不良的生存时间有关。其他多变量Cox回归分析表明,miR-145甲基化是NSCLC患者生存不良的独立预后因素。此外,我们发现通过miR-145直接靶向粘蛋白1,恢复miR-145表达可抑制NSCLC的增殖,迁移和侵袭。我们的结果表明,由于甲基化,低的miR-145表达通过靶向粘蛋白1促进NSCLC细胞增殖,迁移和侵袭。因此,miR-145可能是NSCLC的重要治疗靶标。

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