Xu Bin, Sun Yinghao, Tang Gusheng, Xu Chuanliang, Wang Linhui, Zhang Yuxi, Ji Jiatao
Department of Urology, Changhai Hospital, 174 Changhai Road, Shanghai 200433, China.
Department of Urology, Changhai Hospital, 174 Changhai Road, Shanghai 200433, China.
Cancer Lett. 2009 Jun 18;278(2):220-229. doi: 10.1016/j.canlet.2009.01.007. Epub 2009 Feb 7.
This study discovered that Id-1 expression in androgen-dependent prostate cancer decreased immediately after androgen deprivation but increased after longer androgen deprivation both in vivo and in vitro. Id-1 expression in androgen-independent LNCaP cells was about 6 fold as that in their parental cells. As was the case with LNCaP cells, when androgen receptor (AR) was introduced into AR-negative PC-3 cells, dihydrotestosterone inhibited while flutamide increased Id-1 expression. Thus, Id-1 expression in androgen-dependent prostate cancer was negatively regulated by androgen in a receptor-dependent way. The re-increased Id-1 might partially contribute to the emergence of androgen-independent prostate cancer after longer androgen deprivation therapy.
本研究发现,雄激素依赖性前列腺癌中Id-1的表达在去势后立即下降,但在体内和体外长期去势后均升高。雄激素非依赖性LNCaP细胞中Id-1的表达约为其亲代细胞的6倍。与LNCaP细胞情况相同,当将雄激素受体(AR)导入AR阴性的PC-3细胞时,二氢睾酮抑制而氟他胺增加Id-1的表达。因此,雄激素依赖性前列腺癌中Id-1的表达以受体依赖的方式受到雄激素的负调控。Id-1的再次升高可能部分促成了长期雄激素剥夺治疗后雄激素非依赖性前列腺癌的出现。