姜黄素对雄激素非依赖性前列腺癌细胞Notch信号通路的影响

目的 观察姜黄紊(Curcumin,Cur)对雄激素非依赖性前列腺癌细胞株PC3体外生长及Notch信号通路的影响.方法 应用噻唑蓝(MTT)法、流式细胞术、透射电镜、RT-PCR法观察了6.25、12.5、25.0、50.0 μmol/L浓度姜黄素对PC3细胞生长及Notch1 mRNA和蛋白,Jagged1、Hes1mRNA表达的影响.结果 姜黄素以剂量和时间依赖性方式抑制PC3细胞的生长(F6.25=17.840,F12.5=20.479,F25=99.091,F50=8.40,F24=1081.70,F48=51.495,F72=155.24,P均＜0.01);诱导G2/M期停滞(FS=1708.20,FG2/M=1580.40,P均＜0.01);促进凋亡(F=208.23,P＜0.01);随着Cur梯度浓度引起Notchl、Hesl mRNA分别增高(F=4.872,P＜0.05;F=29.562,P＜0.01),Notch1蛋白表达升高(F=4.579,P＜0.05),JaggedlmRNA的表达下降(F=74.160,P＜0.01).结论 姜黄素能上调Notch1、Hes1,下调Jaggnd1的表达,激活Notch信号通路,是其发挥抗前列腺癌的机制之一.

Effects of curcumin on notch signaling pathway in androgen-independent prostate cancer cell line PC3 in vitro

Objective To investigate the effects of eurcumin (Cur) on growth and Notch signa-ling pathway in androgen-independent prostate cancer cell line (PC3) in vitro. Methods MTT, flow cy-tometry (FCM), electronic microscopy and semiquantitative RT-PCR methods were used to observe the effects of 0,6.25,12.5,25.0,50.0 μmol/L Cur on growth of PC3 cells, and the expression of Notchl,Jagged1 and Hes1 mRNA and Notch1 protein in vitro. Results The growth of PC3 cells was suppressed obviously by Cur in a dose-and time-dependent manner (F6.25 = 17.840, F=12.5 = 20.479 ,F25 = 99.091, F50= 8.40, F24= 1081.70, F48 = 51.495, F72 = 155.24, allP＜0.01). Cur could induce the arrest of PC3cells at G2/M phase in a dose-dependent manner ( FS= 1708.20, FG2/M = 1580.40, P＜0.01), and pro-mote the apoptosis ( F = 208.23 ,P＜0.01 ). Cur could cause characteristic morphological changes of apop-tosis in PC3 cells after 24 h. Compared with control group,the expression of Notch1 and Hes1 mRNA and Notchl protein in PC3 cells treated with Cur for was markedly increased F = 4. 872, P＜0. 05 ; F=29.562,P＜0.01 ;F =4.579,P＜0.05 respectively) ,and the expression of Jagged1 mRNA was declined(F = 74.160,P＜0.01) in a dose-dependent manner. Conclusion Cur could up-regulate the expression of Notch1 and Hes1 and down-regulate the expression of Jaggedl in dose-dependent manner, suggesting the activation of the Notch signaling pathway is probably one of the mechanisms by which Cur suppressed prostate cancer.