vector and co-transfected these reporters with miR-150-3p mimics in NSCLC cells. We tested the expression levels of SRCIN1 and miR150-3p in 163 NSCLC tumor tissues and the results demonstrated that… Click to show full abstract
vector and co-transfected these reporters with miR-150-3p mimics in NSCLC cells. We tested the expression levels of SRCIN1 and miR150-3p in 163 NSCLC tumor tissues and the results demonstrated that the negative correlation between miR-150-3p and SRCIN1 expression levels. NSCLC cells were transfected with miR-150-3p mimics or miR-150-3p inhibitor.To verify the biological significance of LincRNA00494 on tumor growth, xenograft was carried out via subcutaneous injection with NSCLC cells. Results: LincRNA00494 was down-regulated in tumor tissues compared with adjacent nontumor tissues. The expression of Linc00494 was positively correlated with SRCIN1. Silencing LincRNA00494 in H358 and H1299 cells substantially decreased SRCIN1 expression at mRNA and protein levels, whereas LincRNA00494 overexpression improved SRCIN1 levels. MiR-150-3p significantly decreased the luciferase signals of both LINCRNA00494 and SRCIN1 reporters. And there is negative correlation between miR-150-3p and SRCIN1 expression levels. MiR150-3p could target LincRNA00494 and SRCIN1, in addition, LincRNA00494 modulated the expression of SRCIN1 as a molecular decoy for miR-150-3p. Physiological overexpression of LincRNA00494 decreased cell proliferation of the H358 and H1299 cell lines compared with control by CCK-8 assay. In xenograft, tumor growth from overexpressed LincRNA00494 xenograft was significantly decreased. Conclusion: LincRNA00494 might improve SRCIN1 expression by competing for miR-150-3p, subsequently mediating cell proliferation in NSCLC.
               
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