Fig. 3

Let-7b reverses the effect of COL11A1 over-expression on breast cancer cell migration and invasion. a let-7b target genes predicted by TargetScan database and highly expressed genes in microarrays GSE109169, GSE3744 and GSE26910; b binding sites of let-7b and COL11A1; c COL11A1 mRNA expression in clinical tissues detected by RT-qPCR (n = 86); d Luciferase activity of let-7b and COL11A1; *p < 0.05 vs. NC; e COL11A1 mRNA expression in MCF-7 cells treated with depleted COL11A1 determined by RT-qPCR after 48-h of transfection; f proliferation of MCF-7 cells treated with silenced COL11A1 expression detected by EdU assay after 48-h of transfection (×200); g MCF-7 cell migration ability after COL11A1 knockdown determined by Transwell migration assay (×200); h MCF-7 cell invasion ability after COL11A1 knockdown examined by Transwell invasion assay (×200); i CDX2, E-cadherin and Vimentin protein expression in MCF-7 cells treated with silenced COL11A1 detected by western blot analysis after 48-h of transfection; j COL11A1 mRNA expression in MCF-7 cells with different treatments determined by RT-qPCR after 48-h of transfection; k MCF-7 cells proliferation tested by EdU assay after 48-h of transfection (×200); l MCF-7 cell migration ability (×200); m MCF-7 cells invasion ability (×200); n CDX2, E-cadherin and Vimentin protein expression in MCF-7 cells detected by western blot analysis after 48-h of transfection. *p < 0.05 vs. NC. The above statistics were measurement data, which were expressed as mean ± standard deviation. Except for c which was analyzed by paired t-test, analyses in d–n were carried out using unpaired t-test. Each cellular experiment was performed at least 3 times