PD098059对长春新碱诱导胃癌细胞MGC803凋亡的调节作用

Relationship Between PD 098059 and Apoptosis Induced by Vincrestine in Human Gastric Cancer Cells MGC 803

目的:探讨MAPK/ERK kinase(MEK)抑制剂PD 098059对长春新碱(VCR)诱导胃癌细胞系MGC 803细胞凋亡的影响。方法:用流式细胞术对VCR及PD 098059作用下的细胞进行周期解析,观察细胞周期的变化。结果:通过细胞的周期解析发现VCR和PD 098059共同作用的细胞其凋亡比例为35.61％,显著高于VCR单独作用引起的凋亡(18.41％)(P<0.05)。结论:PD 098059可能通过抑制MAPK的活性、抑制胃癌细胞增殖,对VCR诱导MGC 803细胞的凋亡具有协同作用。

Objective: Our aim was to investigate the effect of MAPK/ERK kinase (MEK) inhibitor ,PD 098059, on apoptosis of MGC 803 cells induced by VCR. Methods: The ceils cycle analysis was determined by flow cytonietric to study apoptosis of MCC 803 cells which were exposed to viricreslinc( VCR) and PD098059. Results: The ratio (35. 61% ) of apoptosis cells treated with VCR and PD 098059 was significantly higher than that of those( 18.42% ) treated with only VCR. (P < 0. 05) Conclusion: PD 098059 may cooperate with VCR in apoptosis of MGC 803 cells by inhibiting the activity of MAPK.