西达本胺对人前列腺癌DU145及PC3细胞凋亡的影响

目的:研究西达本胺对前列腺癌DU145、PC3细胞生长抑制及凋亡调控的作用。方法:设置西达本胺浓度分别为4、8、16、32和64μmol/L的5个处理组和对照组(未加西达本胺),分别处理DU145、PC3细胞不同时间,采用MTT法检测细胞的增殖抑制情况,用倒置显微镜观察细胞形态,用流式细胞仪进行细胞凋亡分析,用免疫印迹法检测细胞内Bax、Bcl-2、caspase-3、caspase-9的表达水平。结果:与对照组比较,西达本胺处理组可使细胞明显变圆、体积缩小、脱壁细胞增多;MTT法检测显示,随着西达本胺浓度的增加和作用时间的延长,对DU145、PC3细胞的增殖抑制作用增强,并呈时间、剂量正相关(P<0.01);流式细胞术显示,对照组和16、64μmol/L西达本胺组细胞凋亡率分别为42.24%、50.23%;随着西达本胺浓度的增加,Bcl-2的表达呈下调趋势,Bax、caspase-3、caspase-9的表达呈上调趋势,呈剂量正相关。结论:西达本胺对前列腺癌DU145、PC3细胞生长具有明显的抑制作用,作用机制可能与Bax、Bcl-2、caspase-3及caspase-9凋亡信号通路有关。

Effects of Chidamide on Apoptosis in Human Prostate Carcinoma DU145 and PC3 Cells

Objective： To investigate the regulatory effect of chidamide on proliferation inhibition and apoptosis in prostate carcinoma DU145 and PC3 cells. Methods： The DU145 and PC3 cells were divided into 5 treatment groups（4, 8, 16, 32 and 64 xmol/L chidamide） and control group. The morphological alterations of DU145 and PC3 cells after treated for chidamide were observed by using inverse microscopy, the inhibition of cell prolifera tion was detected by MTT assay, the cell apoptosis was analyzed by flow cytometry, the protein levels of Bax, Bcl2, caspase3 and caspase9 in carcinoma cells were observed by Western blot assay. Results： After being treated with chidamide, DU145 and PC3 cells grew round and small obviously and were against the wall under the inverse microscopel with the increasing of the concent ration of chidamide and the elongation of the treated time, the DU145 and PC3 ceils growth was inhibited, the inhibition of proliferation of DU145 and PC3 cells in creased in a time and dose dependent manner（P〈0.01）. The apoptotic rates of the control group and 16 and 64 txmol/L chidamide treatment groups were 42.24%, 50.23%, respectively. With the increasing of concent ration of chidamide, the Bax, caspase3 and caspase9 expression was increased in a dose dependent manner（P〈O.01）. Conclusion： Chidamide could significantly inhibit the growth of DU145 and PC3 cells, the induction of apoptosis through up regulating Bax, caspase3 and caspase9 is probably one of it s molecular mechanisms.