Fig. 4: LncRNA SEAS1 sponges miR-3940-3p in the TNBC cells.

A RT-qPCR analysis shows the levels of hsa-miR-3940-3p in the control, SEAS1-silenced, and SEAS1-overexpressing MDA-MB-231 and BT-549 cells. B RT-qPCR analysis shows the expression levels of miR-3940-3p in the breast cancer tissues and normal breast tissues (n = 50). GAPDH was used as the internal control. C Schematic diagram shows the predicted wild-type and mutated binding sites for miR-3940-3p in SEAS1. D RT-qPCR analysis shows the levels of SEAS1 or miR-3940-3p pulled down from the lysates of MDA-MB-231cells with the anti-AGO2 antibody in the RIP assay. E Luciferase activity of the reporter construct containing the wild-type or miR-3940 binding mutant of SEAS1 was measured after cotransfection of the reporter with Negative Control (NC) or miR-3940-3p in MDA-MB-231 and BT-549 cells. F–H CCK8, colony formation, and EdU assays show the proliferation rates of the control, miR-3940-3p overexpressing and miR-3940-3p-depleted MDA-MB-231 cells. I Flow cytometry analysis shows the proportion of apoptotic cells in the control, miR-3940-3p overexpressing and miR-3940-3p-depleted MDA-MB-231 cells. J Transwell assays show the migration and invasion rates of the control, miR-3940-3p overexpressing and miR-3940-3p-depleted MDA-MB-231 cells. The data show an average of three independent experiments. *P < 0.05, **P < 0.01, and ***P < 0.001. Representative data from at least 3 experiments with comparable results are shown.