Research Paper Volume 11, Issue 15 pp 5646—5665

The long noncoding RNA MIR210HG promotes tumor metastasis by acting as a ceRNA of miR-1226-3p to regulate mucin-1c expression in invasive breast cancer

Figure 4. MIR210HG regulates MUC1-C expression by competing for miR-1226-3p. (A) Venn diagrams showing the number of potential miRNAs targeting the same genes (including MUC1-C gene), as predicted by three databases: TargetScan, miRDB and miRTarBase. (B) Ideograph of MUC1-C mRNA. The predicted miR-1226-3p binding site in the MUC1-C 3′-UTR. The sequence of wild-type (WT) and mutant (Mut) miR-1226-3p target sites in the MUC1-C 3′-UTR shown in frame. A point mutation was made in the seed region to block the binding between miR-1226-3p and mRNA, the sequence inside the blue frame is higher in the binding index. (C) qRT-PCR results showed a reverse correlation between MUC-1C mRNA and miR-1226-3p mRNA in IBC tissues. (D) Luciferase reporter assay showed that miR-1226-3p mimic transfection suppressed the luciferase activity of MUC-1C-WT reporter in MDA-MB-231 cells. (E) Rescue experiments confirm the mutual regulation of miR-1226-3p and MIR210HG. (F, G) miR-1226-3p mimics suppressed the expression of MUC-1C protein, whereas miR-1226-3p inhibitors reversed it in breast cancer cells. *p < 0.05.