MicroRNAs can act as tumour suppressors or oncogenes by regulating cellular differentiation, proliferation and apoptosis, and the dysregulation of miRNA is involved in the occurrence and development of NSCLC. Here, we provided evidence that miR‐92b as an oncogene in NSCLC by targeting PTEN/AKT. We found that miR‐92b was up‐regulated in human NSCLC tissues and cell lines. MiR‐92b knockdown suppressed the NSCLC cells proliferation and migration in both in vivo and in vitro models. Conversely, miR‐92b overexpression induced an aggressive phenotype. Moreover, miR‐92b‐mediated regulation of NSCLC cell proliferation and migration depended on binding to PTEN mRNA, which then led to the degradation of PTEN and activation of the downstream AKT signalling pathway. Overall, this study revealed the oncogenic roles of miR‐92b in NSCLC by targeting PTEN/AKT, and provided novel insights for future treatments of NSCLC patients.

中文翻译：

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MicroRNA-92b通过靶向NSCLC中的PTEN / AKT而作为致癌基因。

MicroRNA可通过调节细胞分化，增殖和凋亡而充当肿瘤抑制因子或致癌基因，而miRNA的失调与NSCLC的发生和发展有关。在这里，我们提供了通过靶向PTEN / AKT将miR-92b作为NSCLC中的癌基因的证据。我们发现，miR-92b在人NSCLC组织和细胞系中上调。在体内和体外模型中，MiR-92b敲低抑制了NSCLC细胞的增殖和迁移。相反，miR-92b过表达诱导侵略性表型。此外，miR-92b介导的NSCLC细胞增殖和迁移调控取决于与PTEN mRNA的结合，然后导致PTEN降解和下游AKT信号通路的激活。总体而言，这项研究通过靶向PTEN / AKT揭示了miR-92b在NSCLC中的致癌作用，