三氧化二砷诱导胰腺癌细胞系PC-3凋亡及其抑制转移的作用

Effects of arsenic trioxide on the pancreatic carcinoma cell line PC-3 and inhibitory migration

目的:探讨三氧化二砷(亚砷酸,As_2O_3)注射液诱导人类胰腺癌细胞凋亡及其抑制转移的作用机制.方法:用As_2O_3处理人胰腺癌细胞株PC-3,通过流式细胞仪观察细胞的凋亡率及生长周期的变化;用免疫组织化学的方法,检测凋亡相关基因蛋白Fas,Fas-L,Bcl-2和Bax及转移相关基因蛋白CD44和nm23表达的变化.结果:流式细胞仪检测显示明显的凋亡峰出现,并使细胞周期主要被阻滞在S期(14.9%-63.7%);免疫组化结果显示,Bcl-2(+++～+),CD44(++++～+)基因的表达下调,Fas(+～+++)、Fas-L(-～+++)及nm23(+～+++)基因的表达上调.结论:As_2O_3注射液可诱导人类胰腺癌细胞株PC-3凋亡并具有抑制转移作用,这可能与调节Bcl-2,Fas,Fas-L及CD44,nm23蛋白的表达有关.

AIM： To explore the effects of A8203 on apoptosis and its inhibitory migration in a human pancreatic carcinoma cell line. METHODS： The human pancreatic carcinoma PC-3 cell line was treated with As203. The rate of apoptosis and the growth cycle of the cell line were investigated by flow cytometry. The expres- sion of gene proteins related to apoptosis （Fas, Fas-L, Bcl-2, and Bax） and metastasis （CD44 and nm23） were observed by immunohistochemistry. RESULTS： A visible apoptotic peak and block- age of the S phase of the cell cycle （14.86%-63.66%） were shown by flow cytometry. Imrnunohistochemical staining indicated that the expressions of Bcl-2 （＋＋＋-＋） and CD44 （＋＋＋＋-＋） were down regulated, while the expressions of Fas （＋-＋＋＋）, Fas-L （--＋＋＋） and nm23 （＋-＋＋＋） were up-regulated. CONCLUSION： Injections of As203 can induce human pancreatic carcinoma cell apoptosis and inhibit pancreatic carcinoma migration. The mechanism was thought to be that As203 regulated the expression of Fax, Fax-L, Bcl-2, CD44 and nm23.