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. 2020 Jun 2;57(2):466–477. doi: 10.3892/ijo.2020.5076

Figure 4.

Figure 4

LncRNA CASC7 acts as a competing endogenous RNA for miR-92a in NSCLC cells. (A) Predicted miR-92a-binding sites on CASC7. (B) The miR-92a expression levels in 80 paired NSCLC and adjacent tissues were determined by RT-qPCR. P<0.01 vs. normal tissues. (C) RT-qPCR analysis of miR-92a expression levels in NSCLC cells (A549, H358 and H2170) and one normal human bronchial epithelial cell line (16HBE) that was used as a control. Data are presented as means ± standard deviation from three independent experiments; **P<0.01 vs. 16HBE cells. (D and E) The relative miR-92a expression in A549 and H358 cells transfected with si-CASC7 or pcDNA-CASC7 was analyzed by RT-qPCR. Data are presented as means ± standard deviation from three independent experiments; **P<0.01 vs. si-Scramble or pcDNA-vector. (F) The Spearman's rank test was used to analyze the association between CASC7 and miR-92a expression levels in NSCLC tissues (r:-0.8709, P<0.01). (G) RT-qPCR analysis of miR-92a expression levels in A549 and H358 cells following miR-92a mimics or miR-92a inhibitor transfection. (H) Luciferase reporter assay in 293T cells co-transfected with the reporter plasmid (or the corresponding mutant reporter) and the indicated miRNAs. miR-92a mimics significantly decreased the luciferase activity in wt-CASC7 but not in mut-CASC7. Data are presented as means ± standard deviation from three independent experiments, **P<0.01 vs. mimics NC, ##P<0.01 vs. inhibitor NC. NSCLC, non-small cell lung cancer; RT-qPCR, reverse transcription-quantitative PCR; wt, wild-type; mut, mutant.