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. 2012 Jun 25;7(6):e39520. doi: 10.1371/journal.pone.0039520

Figure 6. MiR-21 regulated EMT and CSC phenotype through mediating AKT and ERK1/2 activation.

Figure 6

Established MDA-MB-231/anti-miR-21 cells were transfected with hsa-miR-21 mimics at a concentration of 40 nmol for 72 h. Then the cells were trypsinized, and treated with LY294002 (20 µmol/l) or U0126 (10 µmol/l) for 24 h. (A-E) The relative protein levels of p-AKT and AKT (A), p-ERK and ERK (A), EMT markers (B), CSC surface markers (C), as well as PTEN (D) from blank control, LY294002, and U0126 treatment groups were shown, and semi-quantified (E) as stated before. Beta-actin or GAPDH was used as loading control. (*indicates p<0.05; ★ indicates p<0.001; ▴ indicates p>0.05). (F) The effects of antagonism of miR-21, re-expression of miR-21, LY294002, and U0126 on cell proliferation by cell count (A vs. B, p = 0.0077; B+C vs. B+D, p = 0.0091; B+D vs. B+D+E, p = 0.0109; B+D vs. B+D+F, p = 0.0031).