Fig. 1: TMEM170B as a direct target of miR-27a, is downregulated in breast cancer

a Expression profiles of miRNA-27a in primary breast cancer and normal breast tissues of published GEO profiles (NCBI/GEO/GSE 26659/40525/68085). b Differential expression of miR-27a in breast cancer and paired adjacent noncancerous tissues from the TCGA database. c Kaplan–Meier survival analysis of the overall survival in 1071 BRCA patients with different miR-27a expression. d The miR-27a expression of the breast cancer cells were detected by real-time PCR. e, f Cell proliferation of MCF7 cells transfected with miR-27a mimic (e) or MDA-MB-231 cells with miR-27a inhibitor (f). g, h Cell migration assays of MCF7 cells transfected with miR-27a mimic (g) or MDA-MB-231 cells with miR-27a inhibitor (h). i, j The schematic sequence of constructs used in the dual-luciferase reporter assay and the potential miR-27a binding site with TMEM170B. k The luciferase reporter activity in 293T cells transfected with miR-27a mimic or control and luciferase reporters containing TMEM170B wild type or mutant. l RNA pull-down analysis of relative fold enrichment of TMEM170B using biotin-labeled miR-27a or fold enrichment of miR-27a using biotin-labeled TMEM170B. m, n Relative enrichment of miR-27a and TMEM170B in the RIP assay using anti-Ago2 antibody. o Differential expression of TMEM170B between breast cancer and paired adjacent noncancerous tissues in the TCGA database. p The correlation of TMEM170B and miR-27a expression in TCGA cohort. q, r Kaplan–Meier survival analysis of the overall survival in 1071 BRCA patients with different TMEM170B expression (q) or miR-27a/TMEM170B expression patterns (r). All of the data show mean ± S.E.M. *P < 0.05 vs. CTRL, **P < 0.01 vs. CTRL, ***P < 0.001 vs. CTRL