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. 2019 Jun 21;11:5557–5572. doi: 10.2147/CMAR.S203060

Figure 5.

Figure 5

IRF6-mediated PIK3R2 expression modulates PI3K/AKT pathway to involve in breast cancer pathogenesis. (A) The mRNA expression levels of PIK3R2 in breast cancer and non-cancerous breast cancer tissues were determined by RT-qPCR. (B) PIK3R2mRNA levels were negatively correlated with IRF6 expression in breast cancer tissues as assessed by RT-qPCR (Pearson’s analysis, r=−0.4228; p<0.05). (C) Protein expression levels of p-AKT, AKT, and CD44 in MCF7 and MDA-MB-231 cells were assessed by immunoblotting analysis. GAPDH was used as a reference control. (D) Effect of IRF6 on the expression level of proteins involved in p85β-activated AKT signaling cascades. For the immunoblot analysis of IRF6, p85β, p-AKT, AKT, p-mTOR and mTOR in transient overexpression or suppression of IRF6 cell lines. GAPDH was used as a loading control. (E–G) MDA-MB-231 cells were supplemented with increasing doses of an AKT inhibitor (LY294002) and calculated the number of spheres generated between cells seeded with LY294002 and DMSO. (H and I) IRF6 knockdown cells (sh1) and shRNA control cells treated with DMSO vehicle control and increasing doses of an AKT inhibitor (LY294002); compared to control cells, sh1 cells showed increased sensitivity to LY294002. Data represent the mean±SD, *p<0.05,**p<0.01.