摘要
目的研究吉西他滨体外对人胰腺癌CaPan-1细胞生长的作用及机制。方法将CaPan-1细胞暴露于浓度分别为1、5、10、15μmol/ml的吉西他滨10μl中,RT-PCR法检测细胞中PUMA、bax、bcl-2和c-myc mRNA的表达,MTT检测细胞存活率,流式细胞仪检测细胞凋亡。结果吉西他滨促进CaPan-1细胞凋亡,抑制细胞生长,并有明显的剂量依赖性;药物处理的细胞凋亡伴有PUMA mRNA和c-myc mRNA上调,而bcl-2 mRNA和bax mRNA无明显变化。结论吉西他滨通过促进体外CaPan-1细胞凋亡而抑制其生长,其诱导凋亡与表达上调的PUMA和c-myc的协同作用有关。
Objective To investigate the effect of proliferation and apoptosis and its mechanism of human pancreatic cancer treated by gemcitabine. Methods CaPan-1 cells were treated with serial concentrations （1,5,10 and 15μmol/ml） of gemcitabine.MTI＇ assay was used to observe the inhibitory actions of gemcitabine on CaPan-1 cells. The apoptotic rate of cells were detected by flow cytometry. The expression of apoptosis-related gene（PUMA, c-myc,bax, bcl-2） were detected by RT-PCR. Results The inhibitory action of cell growth was seen in CaPan-1 cells dealt with gemcitabine. It could also promote the occurrence of apoptosis. Gemcitabine inhibited the proliferation of CaPan-1 cells in a concentration- dependent manner. The apoptosis induced by gemcitabine was accompanied by the up-regulation of PUMA and c-myc, but the bax and bcl-2 did not change. Conclusion Gemcitabine can depress the proliferation of CaPan-1 cells in vitro, mainly through the induction of apoptosis,and it is a potential agent for pancreatic cancer chemotherapy, the mechanism is probably related to its effect on the regulation of PUMA and c-myc expression
出处
《苏州大学学报（医学版）》
CAS
北大核心
2007年第6期848-851,共4页
Suzhou University Journal of Medical Science
基金
卫生部科学研究基金(WKJ 2004-2-011)
