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. 2016 Jan 29;11(3):2001–2008. doi: 10.3892/ol.2016.4161

Figure 1.

Figure 1.

BCL9 is a direct target of miR-30c in PCa cells. (A) The sequence alignment of miR-30c, with the ‘seed’ binding sequences on the 3′-UTR region of BCL9 mRNA. (B) Reverse transcription-quantitative polymerase chain reaction verification of induced ectopic expression of miR-30c in DU145 cells following transduction of miR-30c or miR-NC (negative control). (C and D) Western blot analysis confirmed that proteins of multiple target genes of the Wnt/β-catenin pathway, including c-Myc, CD44, SOX9 and BCL9, were substantially downregulated in miR-30c-expressing DU145 cells. β-actin was used as an internal loading control. (D) Quantification of western blot revealed that ectopic expression of miR-30c significantly inhibited BCL9 protein levels in DU145 cells. (E) Luciferase activity was detected following transfection of FLuci vector (3-UTR-BCL9wt FLuci or 3-UTR-BCL9mut FLuci vectors) into miR-30c- or miR-NC-transfected DU145 cells. **P<0.01. CMV, cytomegalovirus; BCL9, B-cell lymphoma 9; miR, microRNA; PCa, prostate cancer; 3-UTR, 3-untranslated region; wt, wild type; mut, mutated.