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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 6. Pharmacological inhibition of Akt in TRAMP mice and genetic deletion of Akt1 in human prostate cancer cells promote epithelial to mesenchymal transition (EMT).

Figure 6

(A) Bar graph showing changes in the mRNA expression of genes regulating EMT in 31 week old TRAMP mice prostate tissues treated with 1mg/kg/day Akt inhibitor TCBN for 6 weeks (n=3). (B) Representative Western blot images of prostate tissue lysates isolated from 31 week old, 6 week TCBN (1mg/kg/day) treated TRAMP mice showing changes in the protein expression of epithelial and mesenchymal markers compared to DMSO treated controls. (C) Bar graphs showing average fold-changes in the expression levels of mesenchymal markers N-Cadherin and Snail, and epithelial marker E-cadherin in prostate tissue lysates isolated from 31 week old, 6 week TCBN treated TRAMP mice compared to DMSO treated controls (n=4). (D) Representative Western blot images of Akt1 knockdown human PC3 and DU145 cell lysates showing changes in the expression levels of epithelial marker E-cadherin and mesenchymal marker N-Cadherin compared to ShControl cells. (E) Bar graph showing average fold-change in the expression levels of epithelial marker E-Cadherin in Akt1 knockdown DU145 cell lysates compared to ShControl cell lysates (n=4). (F) Bar graphs showing average fold-change in the expression levels of mesenchymal markers N-Cadherin in Akt1 knockdown PC3 (left) and DU145 (right) cell lysates compared to respective control cell lysates (n=4). Data presented as Mean ± SD; *P < 0.05.