Fig. 4

LncRNA BCRT1 acts as a sponge of miR-1303 in breast cancer. a Schematic diagram representing the predicted binding sites for miR-1303 in lncRNA BCRT1 and mutant sequences of the potential miR-1303 binding sites. b Luciferase assays in HEK293T cells cotransfected with wild-type or mutant lncRNA BCRT1 and miR-1303 or NC. The data are shown as the means ± SD of triplicate samples. c Anti-AGO2 RIP was performed in HEK293T cells, followed by RT-PCR to detect the expression of lncRNA BCRT1 or miR-1303 associated with AGO2. d RT-PCR was used to detect the effect of lncRNA BCRT1 knockdown on the expression of miR-1303 in breast cancer cells. e The overexpression of miR-1303 in breast cancer cells was validated by RT-PCR. f The proliferation of breast cancer cells transfected with NC or miR-1303 was measured by MTT assay. g MDA-MB-231 and MDA-MB-468 cells were transfected with miR-1303 mimics or NC, and the apoptotic rates were determined by FACS analysis. Representative results are shown, and data are presented as the mean ± SD. h Transwell assays were used to measure the migration of breast cancer cells transfected with miR-1303 mimics or NC. i The effects of lncRNA BCRT1 and miR-1303 cotransfection on cell proliferation were measured by MTT assay. j Transwell assay was used to determine the migration of breast cancer cells cotransfected with lncRNA BCRT1 and miR-1303. k Overexpression of miR-1303 inhibited the effect of conditioned medium from lncRNA BCRT1-overexpressing cells on the tube formation of HUVECs. (*P < 0.05, **P < 0.01, and ***P < 0.001)