Abstract
BackgroundNon‐small cell lung cancer (NSCLC) is a major type of lung cancer with high morbidity and high mortality. miR‐874 has been determined to play a role in tumor suppression in several cancers. The purpose of our study was to detect the biological mechanisms of miR‐874 and AQP3 in NSCLC. Methods: CCK‐8 and Transwell assays were utilized to perform cell invasion.Western blot was employed to evaluate the protein expression. Results: The expression of miR‐874 was lower in NSCLC tissues than that of corresponding adjacent nontumor tissues. Downregulation of miR‐874 predicted a poor prognosis in NSCLC. The cell proliferation and mobility were suppressed by overexpression of miR‐874, which were promoted by knockdown of miR‐874 in A549 and H1299 cells. miR‐874 mediated the expression of AQP3 by directly binding to the 3′‐untranslated regions (UTR) of AQP3 mRNA in NSCLC cells. Moreover, miR‐874 inhibited the proliferation and mobility by targeting AQP3 and inhibited the PI3K/AKT signaling pathway in A549 cells. miR‐874 inhibited the growth of NSCLC in vivo. Conclusions: In conclusion, miR‐874 inhibited proliferation and mobility by regulating AQP3 in NSCLC. The newly identified miR‐874/AQP3 axis provides novel insight into the pathogenesis of NSCLC.
Highlights
Lung cancer is the most frequent cancer with the highest morbidity and mortality worldwide, which includes small cell lung cancer and non-small cell lung cancer (NSCLC).[1]
Transwell assay indicated miR-874 acts as Non-small cell lung cancer (NSCLC) tumor suppressor that cell mobility ability was inhibited by overexpression of miR-874 (P < 0.05) whereas it was enhanced by the miR874 inhibitor (P < 0.05) in A549 and H1299 cells (Fig 2d)
All the results demonstrated that the proliferative and mobility abilities were suppressed by miR-874 in NSCLC cell lines A549 and H1299
Summary
Lung cancer is the most frequent cancer with the highest morbidity and mortality worldwide, which includes small cell lung cancer and non-small cell lung cancer (NSCLC).[1]. MicroRNAs (miRNAs), 19–25 nucleotides long, noncoding RNA, regulate cell development and progress by directly binding to the 30-untranslated regions (UTR) of target mRNAs at post-transcriptional level.[3,4,5] miRNAs may act as tumor suppressors or oncogenes to regulate cancer development in NSCLC, including miR-1258, miR-1269a, miR-1179 and miR-550a.6–9. The purpose of our study was to detect the biological mechanisms of miR-874 and AQP3 in NSCLC. MiR-874 mediated the expression of AQP3 by directly binding to the 30-untranslated regions (UTR) of AQP3 mRNA in NSCLC cells. MiR-874 inhibited the proliferation and mobility by targeting AQP3 and inhibited the PI3K/AKT signaling pathway in A549 cells. Conclusions: In conclusion, miR-874 inhibited proliferation and mobility by regulating AQP3 in NSCLC. The newly identified miR-874/AQP3 axis provides novel insight into the pathogenesis of NSCLC
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