Background The failure of endocrine treatment for advanced prostate cancer might be related to aberrant activation of androgen receptor (AR) Prostate cancer cell line LNCaP contains AR that can be activated by androgen, estrogen and progesterone This study was set to investigate the effects of antisense AR RNA on growth of LNCaP cultured in medium containing varied concentrations of R1881, 17β-estradiol, and progesterone, respectively Methods LNCaP cells transfected with antisense AR RNA retroviral vector pL-AR-SN were designated as LNCaP as-AR . LNCaP cells containing empty vector pLXSN served as LNCaP Neo . LNCaP and LNCaP Neo were taken as controls In vitro cell growth assay, proliferative cells of LNCaP and tranfected LNCaPs were counted by typan staining when they cultured with synthetic androgen R1881, 17β-estradiol, and progesterone, respectively Results Growth of LNCaP as-AR was inhibited significantly ( P <0 05) compared with that of LNCaP and LNCaP Neo at 1 nmol/L R1881, 10 nmol/L 17β-estradiol, and 1 nmol/L progesterone, respectively No difference was seen between LNCaP and LNCaP Neo ( P >0 05) Microscopic observation showed that LNCaP and LNCaP Neo cells grew well, but only few LNCaP as-AR cells were alive Conclusions Our observations indicate that antisense AR RNA retroviral vector pL-AR-SN could change androgen-independent characteristics of LNCaP cells, which might shed some novel insights into the treatment of androgen-independent prostate cancer Background The failure of endocrine treatment for advanced prostate cancer might be related to aberrant activation of androgen receptor (AR) Prostate cancer cell line LNCaP contains AR that can be activated by androgen, estrogen and progesterone This study was set to investigate the effects of antisense AR RNA on growth of LNCaP cultured in medium containing varied concentrations of R1881, 17β-estradiol, and progesterone, respectively Methods LNCaP cells transfected with antisense AR RNA retroviral vector pL-AR-SN were designated as LNCaP as-AR. pLXSN served as LNCaP Neo. LNCaP and LNCaP Neo were taken as controls In vitro cell growth assay, proliferative cells of LNCaP and tranfected LNCaPs were counted by typan staining when they cultured with synthetic androgen R1881, 17β-estradiol, and progesterone, respectively Results Growth of LNCaP as-AR was inhibited significantly (P <0 05) compared with that of LNC aP and LNCaP Neo at 1 nmol / L R1881, 10 nmol / L 17β-estradiol, and 1 nmol / L progesterone, respectively No difference was seen between LNCaP and LNCaP Neo (P> 0 05) Microscopic observation showed that LNCaP and LNCaP Neo cells grew well, but only few LNCaP as-AR cells were alive Conclusions Our observations indicate that antisense AR RNA retroviral vector pL-AR-SN could change androgen-independent characteristics of LNCaP cells, which might shed some novel insights into the treatment of androgen -independent prostate cancer