Fig. 5

miR-29c directly targeted DNMT3B and regulated the DNMT3B/TIMP3/STAT1/FOXO1 pathway in breast cancer cells. a The potential binding site of miR-29c in the 3′UTR of DNMT3B. b Dual-Luciferase Reporter Assay of miR-29c and DNMT3B in MDA-MB-231 cells. c Protein levels of DNMT3B, TIMP3, STAT1, and FOXO1 detected by Western blotting in MCF-7 cells after the transfection of miR-29c inhibitor. d qMS-PCR assay of the methylation level of TIMP3 in MCF-7 cells after the transfection of miR-29c inhibitor. e Protein levels of DNMT3B, TIMP3, STAT1, and FOXO1 detected by Western blotting in MDA-MB-231 cells after the transfection of miR-29c mimic. f qMS-PCR assay of the methylation level of TIMP3 in MDA-MB-231 cells after the transfection of miR-29c mimic. g Migration assays of MCF-7 cells that were co-treated with fludarabine (STAT1 inhibitor) and miR-29c inhibitor. h Invasion assays of MCF-7 cells that were co-treated with fludarabine (STAT1 inhibitor) and miR-29c inhibitor. i Protein levels of STAT1 and FOXO1 detected by Western blotting in MCF-7 cells that were co-treated with fludarabine (STAT1 inhibitor) and miR-29c inhibitor. Data are presented as mean ± SD from three independent experiments, and every experiment was repeated three times, *P < 0.05, ***P < 0.001