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目的探讨米非司酮(MIF)对前列腺癌PC-3细胞周期及其调控蛋白的影响及其作用机制。方法MTT法检测1、10、50、100μmol／L MIF作用于PC-3细胞24-120 h的吸光度(A)值,流式细胞仪检测10、50μmol／L MIF作用PC-3细胞48 h后细胞周期的变化,免疫组化法和Western blot法检测10、50μmol／L MIF处理48 h后PC-3细胞cyclin D1、bax、bcl-2蛋白表达的变化情况。结果1μmol／L MIF作用24-120 h的A值与对照组相比差异无统计学意义(P>0．05);10、50、100μmol／L组A值与对照组比较差异有统计学意义(P<0．01);MIF对PC-3细胞的抑制作用呈时间-剂量依赖性。MIF作用48 h后使PC-3细胞停滞于G1／G0期,并使此期细胞比例从对照组的27．4％增加到10μmol／L组的50．4％和50μmol／L组的59．2％,差异有统计学意义(P<0．05)。处理后PC-3细胞中bcl-2蛋白和cyclin D1蛋白表达量,与对照组比较差异有统计学意义(P<0．05);而bax表达量显著增加。结论MIF以时间-剂量依赖性方式抑制前列腺癌PC-3细胞的增殖,可能通过下调cyclin D1蛋白表达,阻止PC-3细胞G1期向S期的转换,使其停留于G1／G0期;同时降低bcl-2蛋白的表达及激活bax蛋白的表达等抑制前列腺癌PC-3细胞增殖。
Objective To investigate the effect of mifepristone (MIF) on the cell cycle and regulatory protein of PC-3 in prostate cancer and its mechanism. Methods MTT assay was used to determine the absorbance (A) of PC-3 cells treated with 1, 10, 50 and 100μmol / L MIF for 24-120 h. The proliferation of PC-3 cells was detected by flow cytometry The changes of cell cycle, the expression of cyclin D1, bax and bcl-2 in PC-3 cells were detected by immunohistochemistry and Western blot 48 h after treatment with 10 and 50 micromol / L MIF. Results There was no significant difference in A value between 24 and 120 h after 1 μmol / L MIF treatment (P> 0.05). The A value in 10, 50 and 100 μmol / L groups was significantly different from that in control group (P <0.01). The inhibitory effect of MIF on PC-3 cells was time-and dose-dependent. 48 hours after MIF, PC-3 cells were arrested in G1 / G0 phase and the proportion of cells in this phase was increased from 27.4% in control group to 50.4% in 10μmol / L group and 59% in 50μmol / L group. 2%, the difference was statistically significant (P <0.05). Compared with the control group, the expression of bcl-2 protein and cyclin D1 protein in PC-3 cells after treatment was significantly different (P <0.05), while the expression of bax was significantly increased. Conclusions MIF inhibits the proliferation of PC-3 cells in a dose-dependent manner in a dose-dependent manner. MIF may inhibit the transition of G1 phase to S phase of PC-3 cells by down-regulating the expression of cyclin D1, Reduce the expression of bcl-2 protein and activate the expression of bax protein and so on to inhibit the proliferation of prostate cancer PC-3 cells.