Fig. 4

The targeted regulation of TFAP2C by miR-136-5p and miR-198 in SKBR3 and BT-474 cells. A, B Detection of miR-136-5p and miR-198 expressions in HER2-positive breast cancer tissues and the adjacent normal tissues by qRT-PCR, unpaired two-tailed t-test. C, D Pearson correlation analysis of the correlation between miR-136-5p expression and TFAP2C expression (r =-0.9186, P < 0.001, n = 23), miR-198 expression and TFAP2C expression (r =-0.6613 , P < 0.001, n = 23) in HER2-positive breast cancer tissues, Pearson r correlation test. E The binding sites between miR-136-5p and TFAP2C were predicted by online bioinformatics software (RNAInter). F Dual-luciferase reporter gene assay was applied to prove the interaction between miR-136-5p and TFAP2C, unpaired two-tailed t-test. G Online bioinformatics software (RNAInter) analysis discovered that there were binding sites between miR-198 and TFAP2C. H The interaction between miR-198 and TFAP2C was confirmed by a dual-luciferase reporter gene assay, unpaired two-tailed t-test. I–L miR-136-5p mimic, miR-136-5p inhibitor, miR-198 mimic or miR-198 inhibitor was transfected into SKBR3 and BT-474 cells. The transfection efficiency was verified by qRT-PCR and the protein level of TFAP2C was quantified by Western blot, unpaired two-tailed t-test. Data are represented as mean ± SD. ***P < 0.001 vs. Normal or mimic NC. ^##P < 0.01, ^###P < 0.001 vs. inhibitor NC