Objective  The present study investigated the biochemical mechanism of docetaxel(Doc) for the treatment of castration-resistant prostate cancer(CRPC).

  Methods  The prostate cancer cell lines PC-3, LNCaP, and CW22-rv1 were grown in vitro.The expression of c-Jun and the androgen receptor(AR), the relationship between their expression levels, and the viability of LNCaP, PC-3, and CW22-rv1 cells after exposure to Doc were studied in vitro by immunoblot, luciferase, and viability assays.Furthermore, the expression of AR mRNA was analyzed by quantitative real-time polymerase chain reaction(RT-PCR).

  Results  Doc therapy elicited different responses in the different cell lines.PC-3 cells were the most sensitive to treatment, whereas a moderate response was observed in CW22-rv1 and LNCaP cells.The sensitivity and response to Doc was negatively correlated with the level of phosphorylated c-Jun(p-c-Jun) expression.Transfection of the c-jun gene into cell lines decreased their response to Doc treatment, whereas cotransfection of the c-jun and AR genes restored the sensitivity of PC-3 to a moderate degree, with 30% viability was 30%.After long-term exposure to bicalutamide(cas), the Doc-treated LNCaP cells demonstrated increased levels of the prostate specific antigen(PSA).Likewise the AR protein levels decreased with increasing AR mRNA expression.

  Conclusion  This study demonstrated that the level of p-c-Jun decreased the response of PC cells to Doc treatment, but the level of AR increases PC cells response to Doc treatment.The increased AR level inhibits c-Jun/p-c-Jun transcriptional, which decreases the protective effects of Doc in PC cells.