FIGURE 1.

PI3K/AKT and MEK/ERK pathways are hyperactivated in docetaxel-resistant metastatic castration-resistant prostate cancer cell lines. (A) Representative Western blot images showing basal protein expression levels in the DU145, DU145-DR, PC3 and PC3-DR cell lines: phosphorylated AKT (p-AKT Ser473), phosphorylated GSK3β (p-GSK3β Ser9), phosphorylated S6 (p-S6 Ser235/236), PTEN, AKT, GSK3β and S6. α-tubulin was used as endogenous control. (B) Representative Western blot images showing basal protein expression levels of phosphorylated ERK1/2 (p-ERK1/2 Thr202/Tyr204), phosphorylated p90RSK (p-p90RSK Ser380), ERK1/2 and p90RSK in the DU145, DU145-DR, PC3 and PC3-DR cell lines. α-tubulin was used as endogenous control. (C) Western blot analysis (left) and bar graphs (right) showing protein expression changes of phosphorylated AKT (p-AKT) and phosphorylated ERK (p-ERK1/2) in DU145 and PC3 cells after treatment with docetaxel (Doce) at 6 and 12 nM, respectively, for 72 h α-tubulin was used as endogenous control. Results shown were obtained from at least three independent biological replicates. p-values were calculated using a two-tailed Student’s t-test. p-value relative to vehicle.