Fig. 3

BCAS2 is the downstream target of miR-382-5p and exerts tumor-promoting functions in NSCLC. A MicroT and RNA22 were used to predict the potential targets for miR-382-5p. B RT-qPCR assay was carried out to analyze the effect of miR-382-5p on the expression of nine candidates in NSCLC cells. C BCAS2 expression in NSCLC cells compared to 16HBE cells and relative expression and protein levels of miR-382-5p in 70 pairs of NSCLC samples were examined by RT-qPCR and western blot assays. D ENCORI was used to predict the binding sites between miR-382-5p and BCAS2. E Luciferase reporter assay was used to confirm the interaction between miR-382-5p and BCAS2. F RIP assay was carried out to detect whether circ_NEK6, miR-382-5p and BCAS2 co-existed in RISCs. G The interference efficiency of miR-382-5p was detected. I RT-qPCR assay was adopted to detect the expression of BCAS2 under difference treatment conditions. J, K NSCLC cell proliferation was tested by colony formation and EdU assays upon BCAS2 silencing. L, M NSCLC cell apoptosis was evaluated by JC-1 assay and flow cytometry analysis upon BCAS2 silencing. N Transwell assay was conducted to assess NSCLC cell migration upon BCAS2 silencing. O The protein levels of MMP2 and MMP9 proteins in cells transfected with sh-BCAS2#1/2 were measured via western blot assay. P Transwell assay was used to detect NSCLC cell invasion upon BCAS2 silencing. All results were displayed as the mean ± SD. **P < 0.01