摘要
目的：探讨PDGF受体酪氨酸激酶抑制剂（STI571）在胰腺癌中的应用厦机制。方法：应用MTT方法检测胰腺癌细胞的生长情况，应用FACS（PI染色及Aranexin染色）分析胰腺癌细胞的周期改变、凋亡发生厦细胞的死亡机制。应用Wesmm blot检测MAPK磷酸化与生长因子受体磷酸化水平。结果：STI571在胰腺癌中的GI50是17—31．5μmol·L^～1，EGF、FGF-2与IGF-1均可刺激胰腺癌细胞的生长，STI571仅能部分阻断生长因子的作用。STI571对MAPK与生长因子受体磷酸化并无影响，对细胞周期亦无影响。结论：STI571对胰腺癌细胞的生长抑制作用不是通过酪氨酸数酶受体途径实现的，其具体机制厦临床应用尚待进一步研宽。
Objective To investigate the potential role of STI571 in pancreatic cancer.Methods The GI50 of STI571 and the effects of SII571 on growth factor actions in pancreatic cell lines were analyzed by the MIT assay. FACS analysis using Annexin and PI staining was carried out to study cycle,apoposis,and cell death. Westem blot analysis was taken to measure MAP kinase and receptor tyrosine kinase phosphorylation. Rasults STI571 inhibited cell proliferafion in pancreatic cancer lines with GI50 concentrations ranging from 17 to 31.5 μnol·L^-1. EGF,IGF-I,and FGF-2 other than PDGF exerted growth stimulatory effects in pancreatic cancer cell lines. S13571 only partialy blocked these effects on cell growth,and did not abrogate the phosphorylaton of both growth factor-induced receptor and MAPK. Conclusion Our data deraonstrate that STI571 inhibits pancreatic cancer growth with high GI50 concentrations thrugh tyrosine-kinase receptor independent pathways.
出处
《东南大学学报（医学版）》
CAS
2006年第2期77-82,共6页
Journal of Southeast University(Medical Science Edition)
关键词
胰腺癌
酸氨酸激酶抑制剂
血小板衍化生长因子
pancreatic cancer
tyrosine kinsse inhibitor
platelet-derived growth factor
