Skip to main content
. 2018 Nov 20;50(11):152. doi: 10.1038/s12276-018-0155-5

Fig. 4. Mechanism dissection of how miR-92a inhibits DAB2IP expression and how ERβ transcriptionally up-regulates miR-92a expression.

Fig. 4

a DAB2IP 3′UTR containing wild-type (WT) or mutant miRNA-binding sites were cloned into the psiCheck2 vector. b We co-transfected miR-92a and psiCheck2-DAB2IP 3′UTR constructs containing WT or mutant miR92a-targeted binding regions into 293 T cells, and the luciferase activity was assayed. c Schematic depiction of the potential ERβ-binding sites on the 5′ promoter region of the C13orf25 gene that could produce the miR-92a. d Expression of C13orf25 in UMUC3 cells with/without oeERβ and J82 cells with/without shERβ were detected by real-time qPCR. e The ChIP assay showed that ERβ could bind to the 4th predicted ERE site in the promoter of the miR-92a host gene. f UMUC3 cells were transfected with a 2.4 kb promoter-pGL3 luciferase reporter plasmid for luciferase activity assay. The Renilla luciferase reporter was used as an internal control for transfection efficiency. Each experiment was performed independently 3 times. In b, d, and f, data are presented as the mean ± SD. *P < 0.05