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Fig. 2 | Cell Communication and Signaling

Fig. 2

From: Akt1 inhibition promotes breast cancer metastasis through EGFR-mediated β-catenin nuclear accumulation

Fig. 2

Activation of EGFR mediates β-catenin nuclear accumulation in Akt1-impaired MCF-7 and MDA-MB-231 cells. (a) Real time PCR analysis of Wnt2b, Wnt3, Wnt5b and Wnt10a mRNA expression in MCF-7, BT-474, MDA-MB-231 and SKBR3 cells after treated with Akt1 siRNA. Note that no significant alteration is observed on Wnt2b, Wnt3, Wnt5b and Wnt10a mRNA expression after treated with Akt1 siRNA for 24 h in these four distinct breast cancer cells. (b) Real time PCR analysis of β-catenin mRNA expression in MCF-7, BT-474, MDA-MB-231 and SKBR3 cells after treated with Akt1 siRNA. Note that no significant alteration is observed on β-catenin mRNA expression after treated with Akt1 siRNA for 24 h in these breast cancer cells. (c) Western blot analysis showed that knockdown of Akt1 enhanced both the phosphorylation at Tyr1068 and the total protein expression of EGFR in MCF-7, BT-474, MDA-MB-231 and SKBR3 cells, n = 5 per group. (d) Western blot analysis showed that Akt1 siRNA-induced β-catenin nuclear accumulation was almost completely blocked by Gefitinib (20 μM) after 24 h co-incubation in MCF-7 and MDA-MB-231 cells, n = 5 per group. (e-g) Transwell assay with Matrigel demonstrated that Gefitinib reversed AKT1 siRNA-induced breast cancer invasion in MCF-7 (e, f) and MDA-MB-231 cells (e, g). *p < 0.05, **p < 0.01, ***p < 0.001, one-way ANOVA, n = 5 per group

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