Fig. 7

miR-3074-5p mediates the tumor-suppressive function of RARαS77A by targeting DHRS3. a Comparison of miRNA expression in RARαS77A-overexpressed and control MDA-MB-231 cells by miRNA sequencing. Each cell was tested in triplicate. b qRT-PCR analysis of miR-3074-5p expression in RARαS77A-overexpressed MDA-MB-231 cells, and MTT analysis of cell proliferation after transfections of control mimic and miR-3074-5p mimic. c Venn diagram displaying miR-3074-5p computationally predicted targets by three different prediction algorithms: miRanda, TargetScan, and miRDB. d qRT-PCR and western blotting analysis of transcriptional and translational levels of DHRS3 after overexpression of either RARαS77A or miR-3074-5p. e Schematic representation of DHRS3 3’UTR demonstrating putative miRNA target site. Relative luciferase activity of co-transfection of miR-3074-5p with the WT 3′-UTR of DHRS3 in 293FT cells. f Kaplan-Meier representations of the probabilities of recurrence-free survival according to the expression levels of DHRS3 in TNBC patients. A log-rank test was used to evaluate significance. g Cells were transiently transfected with p-Enter vector or p-Enter-DHRS3, and the DHRS3 protein level was detected by western blotting. h MTT analysis of cell viability of MDA-MB-231 cells overexpressing wild-type DHRS3 or DHRS3-Y188H mutant, in the presence or absence of different RARs agonists. * p < 0.05, ** p < 0.01, *** p < 0.001