Objective: To explore the inhibitory effect of genistein (GEN) on the proliferation of VCaP castration-resistant prostate cancer (CRPC) cells.
Methods: VCaP CRPC cells were treated with GEN at the concentrations of 0, 12.5, 25, 50, 100, and 200 μmol/L for 24, 48, and 72 hours followed by determination of their proliferation by CCK-8 assay and their cycle by flow cytometry. The expression of Ki-67 in the cells was detected by immunocytochemistry and the levels of PSA, Cyclin D1, PCNA, and P53 determined by Western blot.
Results: After 72 hours of treatment with GEN at 12.5, 25, 50, 100, and 200 μmol/L, the inhibition rates of the VCaP cells were (25.38±0.02)%, (31.14±0.29)%, (45.27±0.03)%, (52.19±0.05)%, and (68.21±0.19)%, respectively, all significantly higher than in the 0 μmol/L group (［10.08±0.02］%)(P<0.05). GEN caused the arrest of the VCaP cells in the G2/M phase (P<0.05) and inhibited the expression of Ki-67. The expressions of PSA, Cyclin D1, and PCNA were gradually down-regulated while that of P53 up-regulated with the increased concentration of GEN (P<0.05).
Conclusions: GEN inhibits the proliferation of VCaP CRPC cells by arresting the cell cycle with related protein expression changes.
目的： 研究染料木黄酮(GDN)对去势抵抗性前列腺癌细胞VCaP增殖的抑制作用及可能机制。方法： 以不同浓度（0、12.5、25、50、100、200 μmol/L）的GEN处理去势抵抗性前列腺癌细胞VCaP，分别在24、48、72 h以CCK-8法测定细胞增殖；以流式细胞术检测细胞周期；以免疫荧光法检测Ki-67表达水平；以Western 印迹法检测Cyclin D1、PCNA、P53及PSA表达水平。结果： 12.5、25、50、100、200 μmol/L GEN作用于VCaP细胞72 h后，对VCaP细胞的抑制率分别为（25.38±0.02）%、（31.14±0.29）%、（45.27±0.03）%、（52.19±0.05）%与（68.21±0.19）%，与对照组［(10.08±0.02)%］相比差异有统计学意义（P<0.05）。流式细胞术显示GEN可导致VCaP细胞G2/M期阻滞（P<0.05）。免疫细胞化学法检测显示GEN能够抑制细胞中Ki-67的表达。Western印迹显示去势抵抗性前列腺癌细胞内PSA、Cyclin D1、PCNA随着GEN浓度的增加逐渐下调，P53随着GEN浓度的增加逐渐上调(P<0.05)。 结论： GEN能够抑制体外培养的去势抵抗性前列腺癌细胞VCaP增殖，其作用机制可能与阻滞细胞周期并伴随相关周期蛋白表达的改变有关。.
Keywords: castration-resistant prostate cancer; genistein; proliferation.