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. Author manuscript; available in PMC: 2013 Dec 30.
Published in final edited form as: Mol Cancer Ther. 2010 May 25;9(6):10.1158/1535-7163.MCT-09-0880. doi: 10.1158/1535-7163.MCT-09-0880

Figure 2.

Figure 2

API-2 blockade of AKT function reduces sCLU expression and induces chemosensitivity to docetaxel in drug-resistant tumor cells. A, DU145-DR and PC3-DR tumor cells were pretreated 2 h with the indicated doses of API-2, a potent AKT inhibitor, and exposed to docetaxel-containing medium for 48 h. Cell lysates were then prepared and analyzed by Western blotting with antibodies against pAKT. The lysates were also probed with antibodies specific for total AKT and sCLU. Treatment with API-2 caused a dose-dependent inhibition of active AKT and sCLU protein expression. B, CWR22Rv1 tumor cells were pretreated 2 h with the indicated doses of API-2 and cultured for 48 h in complete medium. Cell lysates were made and Western blot analysis was done to detect pAKT, total AKT, sCLU, and β-actin. Treatment with API-2 caused a dose-dependent inhibition of active AKT and sCLU protein expression. C, DU145-DR and PC3-DR tumor cells, similarly treated with API-2 for 2 h, were analyzed for cell apoptosis by Annexin V/PI staining after a further 48-h culture in docetaxel medium. Both cell lines succumbed to docetaxel-induced cell death after API-2 treatment to deplete AKT function.