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. Author manuscript; available in PMC: 2018 Aug 28.
Published in final edited form as: Cancer Lett. 2017 Jun 7;402:177–189. doi: 10.1016/j.canlet.2017.05.028

Figure 8. Prostate cancer cell EMT as a result of Akt1 suppression is reliant on reduction in the levels of β-catenin.

Figure 8

(A) Representative Western blot images of control and Akt1 knockdown PC3 and DU145 cell lysates showing changes in the expression levels of β-Catenin and p-β-Catenin compared to respective control cell lysates. (B) Bar graphs showing average fold-changes in the expression levels of β-Catenin and p-β-Catenin in Akt1 knockdown PC3 and DU145 cell lysates compared to respective control cell lysates (n=4). (C) Representative Western blot images of Akt1 knockdown PC3 and DU145 cell lysates showing changes in the expression levels of p-β-Catenin in the presence and absence of β-Catenin transcription inhibitor ICG001 (10 μM) and Wnt signaling inhibitor IWR-1 (10 μM) 72 hours after treatment. (D) Bar graphs showing average fold-changes in the expression levels of p-β-Catenin in Akt1 knockdown PC3 and DU145 cell lysates in the presence and absence of β-Catenin transcription inhibitor ICG001 and Wnt signaling inhibitor IWR-1 (72 hours) (n=4). (E) Representative Western blot images of normal PC3 and DU145 cell lysates showing changes in the expression levels of N-Cadherin in the presence and absence of 10 μM of GSK-3 inhibitor SB415286, β-Catenin transcription blocker ICG001 and Wnt signaling inhibitor IWR-1 (72 hours). (F) Bar graphs showing fold-changes in the expression levels of N-cadherin in PC3 and DU145 cell lysates pre-treated with GSK-3 inhibitor SB415286, β-Catenin transcription blocker ICG001 or Wnt signaling inhibitor IWR-1 (72 hours). (G) Representative Western blot images of DU145 cell lysates showing changes in the expression levels of N-Cadherin after treatment with TGFβ1 (5 ng/ml; 72 hours) alone and in combination with TGFβ receptor inhibitors LY2109761 and SB431542, β-Catenin transcription blocker ICG001 and Wnt signaling inhibitor IWR-1.