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目的:观察索拉非尼对人非小细胞肺癌(non-small cell lung cancer,NSCLC)A549和H1299细胞增殖和凋亡的影响,并探讨其可能机制。方法:不同浓度索拉非尼作用A549和H1299细胞后,应用CCK-8(cellcountingkit-8)法检测细胞的增殖抑制率,FCM检测细胞周期和细胞凋亡,蛋白质印迹法检测细胞的磷酸化细胞外信号调节激酶(phosphorylated extracellular signal-regulated kinase,p-ERK)和磷酸化Ak(tphosphorylated Akt,p-Akt)蛋白的表达水平。结果:不同浓度索拉非尼能抑制A549和H1299细胞的增殖,且呈浓度依赖性(P<0.05);索拉非尼能诱导细胞凋亡,与对照组比较,G0/G1期细胞比率明显上升,S期细胞比率相应下降,细胞阻滞于G0/G1期(P<0.05);索拉非尼作用后,A549和H1299细胞中p-ERK蛋白的表达明显低于对照组(P<0.05)。结论:索拉非尼能抑制人NSCLCA549和H1299细胞的增殖并诱导其凋亡,其作用机制可能与阻断ERK信号通路有关。
Objective: To observe the effect of sorafenib on the proliferation and apoptosis of human non-small cell lung cancer (NSCLC) A549 and H1299 cells and to explore its possible mechanism. Methods: After A549 and H1299 cells were treated with different concentrations of sorafenib, cell proliferation was detected by cell counting kit-8 (CCK-8), cell cycle and apoptosis were detected by FCM, and phosphorylated cells were detected by Western blotting The expression of phosphorylated extracellular signal-regulated kinase (p-ERK) and phosphorylated Akt (p-Akt) protein were detected by RT-PCR. Results: Sorafenib at different concentrations inhibited the proliferation of A549 and H1299 cells in a concentration-dependent manner (P <0.05), and sorafenib induced apoptosis. Compared with the control group, the cell ratio at G0 / G1 phase was significantly higher (P <0.05). After sorafenib, the expression of p-ERK in A549 and H1299 cells was significantly lower than that in the control group (P <0.05) ). Conclusion: Sorafenib can inhibit the proliferation and induce the apoptosis of human NSCLCA549 and H1299 cells, which may be related to the block of ERK signaling pathway.