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. Author manuscript; available in PMC: 2015 Aug 1.
Published in final edited form as: Breast Cancer Res Treat. 2014 Jul 8;146(3):487–502. doi: 10.1007/s10549-014-3040-5

Fig. 4.

Fig. 4

Ectopic expression of miArrest inhibitor of has-miR-17-5p (miR-17IN) in MDA-MB-231 cells (MB231-17IN) resulted in reduced binding to RNA-induced silencing complex (RISC) and elevated expression of target mRNAs. a miR-17IN reduced RISC binding of mRNAs that harbor conserved target sites in their 3′-UTRs with exact match to positions 2–8 of the mature miR-17-5p. RISC binding was examined by AGO2-immunoprecipitation (AGO2-IP) followed by qPCR analysis (upper panel). b miR-17IN increased expression of miR-17-5p target genes at mRNA and protein levels. Expression levels of mRNAs and proteins were examined by qPCR and immunoblotting analysis, respectively. The average fold changes of protein levels from two independent experiments were indicated. c Effect of ectopic expression of miR-17IN on RISC binding and expression of mRNAs that are encoded by pro-metastatic genes and contain miR-17 target sites in their 3′-UTRs. TGFBR2, a validated miR-17 target, is included as a positive control