Research Paper Volume 13, Issue 9 pp 13073—13086

MiR-205 suppressed the malignant behaviors of breast cancer cells by targeting CLDN11 via modulation of the epithelial-to-mesenchymal transition

CLDN11 was a direct target of miR-205. (A, B) The predicted binding sites of miR-205 at the 3’-UTR of CLDN11 using bioinformatics (B, C) Overexpression of miR-205 reduced the luciferase activity of wild-type 3’-UTR of CLDN11 in MCF-7 and MDA-MB-231 cells. (D) Over-expression of miR-205 suppressed both the mRNA and protein levels of CLDN11 in both MCF7 and MDA-MB-231 cells.

Figure 7. CLDN11 was a direct target of miR-205. (A, B) The predicted binding sites of miR-205 at the 3’-UTR of CLDN11 using bioinformatics (B, C) Overexpression of miR-205 reduced the luciferase activity of wild-type 3’-UTR of CLDN11 in MCF-7 and MDA-MB-231 cells. (D) Over-expression of miR-205 suppressed both the mRNA and protein levels of CLDN11 in both MCF7 and MDA-MB-231 cells.