MicroRNA-501-3p (miR-501-3p) has been reported to play tumor-suppressive roles in different cancers; however, its expression pattern and biological function in non-small cell lung cancer (NSCLC) remain unknown. In this study, we noted downregulation of miR-501-3p in NSCLC tissues and cell lines. Functional assays showed that overexpression of miR-501-3p suppressed NSCLC cell proliferation, clonogenicity, migration, and invasion. Moreover, miR-501-3p overexpression attenuated in vivo tumor growth in a nude mouse model. In terms of the mechanism, RAP1A was identified as a novel target of miR-501-3p. Overexpression of RAP1A strongly attenuated the inhibitory effects of miR-501-3p on the capacity of NSCLC cells for proliferation and motility. In the clinical samples of NSCLC, miR-501-3p levels negatively correlated with RAP1A expression, which was upregulated in NSCLC. Collectively, these results indicate that miR-501-3p acts as a tumor suppressor in NSCLC by directly targeting RAP1A mRNA and may serve as a theranostic biomarker for patients with NSCLC.

中文翻译：

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通过下调RAP1A，MiR-501-3p在非小细胞肺癌中起着抑癌作用。

据报道，MicroRNA-501-3p（miR-501-3p）在不同的癌症中起着肿瘤抑制作用。然而，其在非小细胞肺癌（NSCLC）中的表达模式和生物学功能仍然未知。在这项研究中，我们注意到NSCLC组织和细胞系中miR-501-3p的下调。功能分析表明，miR-501-3p的过表达抑制了NSCLC细胞的增殖，克隆形成，迁移和侵袭。此外，miR-501-3p过表达会减弱裸鼠模型中的体内肿瘤生长。在机理上，RAP1A被确定为miR-501-3p的新靶标。RAP1A的过表达强烈减弱了miR-501-3p对NSCLC细胞增殖和运动能力的抑制作用。在NSCLC的临床样本中，miR-501-3p水平与RAP1A表达负相关，在NSCLC中被上调。总体而言，这些结果表明，miR-501-3p通过直接靶向RAP1A mRNA而在NSCLC中起着抑癌作用，并且可以作为NSCLC患者的治疗诊断生物标志物。