mir-614 inhibited lung cancer cell invasion and proliferation via targeting psa

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ID: 211398
2014
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Abstract
Background and objective MicroRNAs (miRNAs) is a group of non-coding small RNA molecules, which play important roles in the development of tumor. The mechanisms of various kinds of miRNAs in lung cancer still need to be further elucidated. This study investigated the function of miR-614 on lung cancer cell invasion and proliferation. Methods Real-time quantitative PCR was used to detect the expression of miR-614 in lung cancer cell PGCL3 and PGLH7. Transwell assay was used to test the role of miR-614 on regulating invasion and migration of cells. CCK8 assay and BrdU incorporation assay was used to assess the role of miR-614 on cell proliferation. Bioinformatics software predicted the potential target genes of miR-614 and dual luciferase reporter gene was used to analyze the binding between miR-614 and 3’UTR of puromycin-sensitive aminopeptidase (PSA). Western blot detected the PSA protein levels. Results The expression of miR-614 in PGCL3 cells with high metastasis potential was significantly lower than that in PGLH7 cells with low metastasis potential. Furthermore, altered expression of miR-614 by transfection of pre-miR-614 mimics and inhibitor significantly affected the ability of invasion and proliferation of lung cancer cells. Bioinformatics analysis predicted that PSA was one of the potential target genes of miR-614. Altered expression of miR-614 markedly down-regulated the PSA protein levels of lung cancer cells. In addition, dual luciferase reporter gene assay indicated that miR-614 regulated PSA expression by binding to the 3’UTR of PSA mRNA. Conclusion MiR-614 inhibited cell invasion and proliferationa targeting PSA in lung cancer cells, PGCL3.
Reference Key
lv2014chinesemir-614 Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors ;Fang LV;Qi XUE
Journal proceedings of the 10th acm multimedia systems conference, mmsys 2019
Year 2014
DOI
10.3779/j.issn.1009-3419.2014.10.02
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