目的: 探讨糖皮质激素地塞米松抑制雄激素非依赖性前列腺癌细胞DU145的机制。方法: 通过细胞培养方法观察地塞米松及其受体阻断剂RU486对前列腺癌DU145细胞增殖的作用；采用流式细胞仪测定地塞米松对DU145细胞细胞周期的影响；利用Western blot技术检测DU145细胞受地塞米松作用后cyclin D1表达水平和ERK1/2活性的变化；用RT-PCR技术检测DU145细胞中糖皮质激素受体mRNA的表达。结果: 地塞米松明显抑制DU145细胞的增殖，并且有剂量依赖效应；地塞米松使细胞周期阻滞于G0/G1期。Western blot结果显示，地塞米松作用DU145细胞3 d后，细胞内ERK1/2的活性降低，cyclin D1表达量下降。RU486可以拮抗地塞米松对DU145细胞的作用效果。RT-PCR结果显示DU145细胞有糖皮质激素受体mRNA的表达。结论: 地塞米松具有抑制前列腺癌DU145细胞增殖和阻滞细胞周期的作用，此作用与其降低ERK1/2活性、抑制cyclin D1合成有关，提示糖皮质激素对前列腺癌的治疗有重要意义。

Objective: To explore the mechanism by which dexamethasone inhibits androgen-independent prostate cancer cells. Methods: The effects of dexamethasone and RU486, a blocker of dexamethasone receptor, on DU145 cell growth were abserved. Flow cytometric analysis was performed to examine the effects of dexamethasone on cell cycle. Western blot analysis was employed to examine the effects of dexamethasone on extracellular signal-regulated kinase 1/2 activity and cyclin D1 expression in DU145 cells. Expression of glucocorticoid receptor gene mRNA was detected by reverse transcriptase-polymerase chain reaction (RT-PCR). Results: Dexamethasone dose dependently inhibited the growth of DU145 cell and caused cell arrest at G0/G1 stage. Western blot indicated that ERK 1/2 activity and cyclin D1 expression were suppressed after 3 d culture with dexamethasone. The effects of dexamethasone were blocked by RU486 when added simultaneously with dexamethasone. RT-PCR showed expression of glucocorticoid receptor mRNA in DU145 cells. Conclusion: Dexamethasone can suppress DU145 cell proliferation and cell cycle, possibly through the decreasing ERK1/2 activity and cyclin D1 expression, indicating glucocorticoid may have potential therapeutic effect on prostate cancer.