Fig. 5

Overexpression of MUC1-C attenuated the effect of curcumin on cell growth inhibition and curcumin-induced phosphorylation of ERK1/2 and SAPK/JNK. a PC3 and DU145 cells were transfected with the control (pCMV6) or expression constructs of MUC1-C for 24 h before exposing the cells to curcumin for an additional 24 h. Afterwards, p65 and MUC1-C protein expression were determined by Western blot. b PC3 and DU145 cells were transfected with the control (pCMV6) or expression constructs of MUC1-C for 24 h before exposing the cells to curcumin for an additional 48 h. Afterwards The cell viability was determined using the MTT assay as described in the Materials and Methods section. Insert on the upper panel represented the protein levels of MUC1-C as determined by Western blot. β-actin was used as internal control. Values in bar graphs were given as the mean ± SD from three independent experiments performed in triplicate. *Indicates significant difference as compared to the untreated control group (P < 0.05). **Indicates significant difference from curcumin treated alone (P < 0.01). c PC3 and DU145 cells were transfected with the control (pCMV6) or expression constructs of MUC1-C for 24 h before exposing the cells to curcumin for an additional 8 h. Afterwards, p-SAPK/JNK and p-ERK1/2 were determined by Western blot. d The diagram the shows that curcumin inhibits the growth of androgen-independent prostate cancer cells through ERK1/2 and SAPK/JNK-mediated inhibition of p65, followed by reducing expression of MUC1-C. There is a synergy of curcumin and bicalutamide. The negative feedback regulatory loop of MUC1-C to ERK1/2 and SAPK/JNK signaling pathways also adds the important role of MUC1-C in mediating the overall responses of curcumin