澳洲茄边碱对前列腺癌细胞增殖的抑制作用及机制研究

Effect and mechanism of solamargine on proliferation of prostate cancer cells

目的研究澳洲茄边碱(solamargine,SM)对人前列腺癌激素非依赖细胞增殖的影响及可能的作用机制。方法用不同浓度SM(0、1、2、4、6、8、10μmol/L)处理DU145和PC3细胞,MTT法检测SM对细胞生长的影响,Western blot检测SM对相关信号通路蛋白p38 MAPK、ERK1/2 MAPK、MUC1表达的影响。结果 6μmol/L SM作用24h后DU145和PC3细胞活力分别为(52.53±9.05)%、(56.28±2.36)%,并具有时间和剂量依赖;10μmol/L SM作用24h后细胞活力分别为(27.36±2.72)%、(32.07±2.53)%。流式细胞术分析显示不同浓度SM(0、4、6、8μmol/L)处理PC3细胞能引起PC3细胞阻滞在G1期,G1期细胞比例分别为(52.61±0.50)%、(52.96±1.49)%、(66.16±2.84)%和(69.03±2.38)%。且能激活MAPK信号通路减少下游蛋白MUC1的表达。结论 SM能明显抑制DU145和PC3细胞生长,该作用可能与MAPK信号通路的激活以及下游MUC1蛋白表达下调有关。

Objective To investigate the effect of solamargine （SM）on the proliferation of prostate cancer cells and the possible mechanism. Methods DU145 and PC3 cells were treated with different concentration of SM （0,1,2,4,6,8,10μmol/L）. MTT assay were used to detect the inhibiting effect of SM on the proliferation of DU145 and PC3. Expression of p38 MAPK, ERK1/2 MAPK,MUC1 protein were detected by Western blot. Cell cycle was detected by flow cy-tometry. Results The cell viability of DU145 and PC3 cells after treated with 6μmol/L SM for 24 h were （52.53±9.05）% and （56.28±2.36）%. With time and dose dependent,when treated with 10μmol/L SM for 24 h were （27.36±2.72）%,（32.07±2.53）%. SM （0,4,6,8μmol/L） can induce cell cycle arrest at G0/G1 phase of PC3 and activate MAPK signal pathway which can re-duce the downstream protein MUC1 expression. The cell rate of G1 were （52.61±0.50）%,（52.96± 1.49）%,（66.16±2.84）% and （69.03±2.38）%,respectively. Conclusions SM can inhibit the growth of DU145 and PC3. The mechanism may be related to the activation of MAPK signal path-way and cut on the downstream MUC1 protein expression.