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舒尼替尼对胃癌细胞BGC-823增殖的影响及机制 被引量:5

Effects and mechanisms of sunitinib on the proliferation of BGC-823
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摘要 探索舒尼替尼对胃癌细胞BGC-823增殖的影响及机制。不同浓度舒尼替尼处理BGC-823细胞24、48、72、96 h后,MTT法检测细胞增殖,得出药物的半数抑制浓度为0.592 8μmol/L。筛选出比较接近半数致死量的3个药物浓度0.25、0.50、1.00μmol/L作用细胞48 h后,细胞核染色检测细胞凋亡;免疫荧光染色法检测Notch-1的表达及细胞凋亡水平;蛋白质免疫印迹检测Notch-1、caspase-3、caspase-9蛋白表达水平。MTT检测结果显示,舒尼替尼在浓度0.156 25~10μmol/L时可显著抑制BGC-823细胞增殖,且具有时间和剂量依赖性。细胞核染色结果显示,不同浓度的舒尼替尼处理BGC-823细胞48 h后随浓度的增加,细胞凋亡数量显著增多。蛋白质免疫印迹结果显示,不同浓度舒尼替尼作用48 h后,Notch-1蛋白的表达水平随浓度的增加而降低,caspase-3、caspase-9表达水平随浓度的增加而升高。舒尼替尼通过抑制Notch-1的信号通路活性,进而抑制BGC-823细胞的增殖并诱导细胞凋亡。 To explore the effects of sunitinib on the proliferation of BCG-823 in gastric cancer cells. Methods : BGC- 823 gastric cancer cells were treated with different concentration sunitinib for 24 h, 48 h, 72 h and 96 h, and cell proliferation was determined by MTT method. The expression of Notch-1 and the level of apoptosis were detected by immunofluorescence staining method. The expressions of Notch-l, caspase-3 and caspase-9 protein were analyzed by Western blotting. Results : MTT results showed that the proliferation of BGC-823 cells could be significantly inhibited by the time and dose dependent manners in the concentrations of 0. 156 25-10 tμmol/L. The results of immunofluorescenee showed that the number of apoptosis increased in the treatment of BCG-823 cells with different concentrations. The results of Western blotting showed that the expression levels of the Notch-1 protein decreased with the different concentrations of sunitinib, and the expression level of caspase-3 was increased accordingly. Conclusion: By inhibiting the signal pathway activity of Notch-l, sunitinib inhibits the proliferation of BGC-823 cells and induces apoptosis.
作者 杨旭 刘春灵 徐宛玲 马永超 Yang Xu;Liu Chunling;Xu Wanling;Ma Yongchao(Luohe Medical College, Luohe 462000, Chin)
出处 《解剖学杂志》 CAS CSCD 2018年第3期268-271,275,共5页 Chinese Journal of Anatomy
基金 河南省科技厅科技攻关项目(152102310219)
关键词 BGC-823 增殖 舒尼替尼 NOTCH-1 caspase-3 CASPASE-9 BCG-823 proliferation sunitinib Notch-1 caspase-3 caspase-9
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