【摘要】 目的检测非小细胞肺癌(NSCLC)细胞株的凋亡以及促凋亡蛋白(BIM)的表达,探讨吉非替尼对其的影响。方法采用Annexin PI单染法检测吉非替尼作用下各细胞株的凋亡,免疫印迹法检测BIM的表达。结果吉非替尼诱导NSCLC细胞株凋亡,其中对H1650、H1975突变株的诱导凋亡率高于A549细胞株(P<0.01),H1650的BIM表达随吉非替尼浓度的增加而增强,H1975的BIM表达较高,但受吉非替尼浓度变化的影响不明显,而A549的BIM表达需要更高浓度的吉非替尼作用。结论吉非替尼可以使NSCLC细胞表皮生长因子受体(EGFR)突变株细胞内的BIM表达增高,并且可能通过上调BIM的表达来诱导肿瘤细胞凋亡。更多还原

【Abstract】 Objective To detect the apoptosis and Bcl-2 interacting mediator of cell death(BIM) expression in non-small cell lung cancer(NSCLC) cells,and analyze the effect of gefitinib on them.Methods Apoptosis of cells treated with different concentrations of gefitinib was measured by Annexin PI.Expression of BIM treated with different concentrations of gefitinib was detected by Western blot.Results Gefitinib could induce apoptosis of NSCLC cell lines.Apoptosis rates of H1650 and H1975 mutant cells were higher than that of A549 cells(P<0.01).Expression level of BIM in H1650 mutant cells was increased with the increase of concentrations of gefitinib,and it was much higher in H1975 cells than that in H1650 cells,but it obviously did not change in A549 cells with different concentrations of gefitinib.A549 cells could express higher BIM if given a higher concentration of gefitinib.Conclusion Gefitinib can increase expression of BIM in NSCLC cells with epidermal growth factor receptor(EGFR) mutation,which may be the main mechanism to induce cell apoptosis.更多还原