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引用本文:纪柯伊,吴宿慧,李根林,远佳瑶,李寒冰.基于PI3K/Akt信号通路探讨L-硒-甲基硒代半胱氨酸对EC9706食管癌细胞的影响[J].中国现代应用药学,2025,42(9):1-7.
Ji Ke-yi,WU Su-hui,LI Gen-lin,YUAN Jia-yao,LI Han-bing.Effects of L-se-methyl Selenocysteine on proliferation, migration and apoptosis of EC9706 esophageal carcinoma cells via PI3K/Akt signaling pathway[J].Chin J Mod Appl Pharm(中国现代应用药学),2025,42(9):1-7.
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基于PI3K/Akt信号通路探讨L-硒-甲基硒代半胱氨酸对EC9706食管癌细胞的影响
纪柯伊, 吴宿慧, 李根林, 远佳瑶, 李寒冰
河南中医药大学 河南郑州
摘要:
目的 研究L-硒-甲基硒代半胱氨酸(Se-methylselenocysteine, L-SeMC)对食管癌EC9706细胞凋亡及凋亡相关蛋白的影响,探讨其诱导细胞凋亡的作用。 方法 不同浓度的L-SeMC(12.5、25、50、100μmol·L-1)RPMI-1640培养液作用于食管癌EC9706细胞24h、48h,MTT法检测L-SeMC对细胞增殖的抑制作用,划痕实验检测不同浓度的L-SeMC(12.5、25、50、100μmol·L-1)的细胞迁移情况,流式细胞仪检测L-SeMC(空白、25、50、100μmol·L-1)的细胞凋亡情况,Western blot法检测Bcl-2,Bax,caspase3蛋白表达,SPSS16.0进行数据录入及统计学分析。结果 L-SeMC对EC9706细胞的增殖具有明显的抑制作用,呈现时间-浓度依赖性(P<0.001),其中100 μmol·L-1浓度抑制作用最明显。48h后,凋亡相关蛋白Bax和caspase3的蛋白表达较空白对照组明显上调(P<0.001),而Bcl-2的蛋白表达较空白对照组明显下调(P<0.001),变化呈浓度依赖性。
关键词:  食管癌  L-硒-甲基硒代半胱氨酸  凋亡
DOI:
分类号:
基金项目:]:河南省科技攻关计划(232102311191);河南中医药大学2022年度研究生科研创新类项目(2022KYCX004)
Effects of L-se-methyl Selenocysteine on proliferation, migration and apoptosis of EC9706 esophageal carcinoma cells via PI3K/Akt signaling pathway
Ji Ke-yi, WU Su-hui, LI Gen-lin, YUAN Jia-yao, LI Han-bing
Henan University of Traditional Chinese Medicine
Abstract:
Objective to investigate the effects of L-se-methylselenocysteine (L-SeMC) on apoptosis and apoptosis-related proteins in esophageal carcinoma cell line EC9706 and its Selenocysteine. Methods: different concentrations of L-SeMC (12.5,25,50,100 μmol · L -1) RPMI-1640 were used to treat EC9706 cells for 24 h and 48 h. the inhibitory effect of L-SeMC on the proliferation of EC9706 cells was detected by MTT assay, the cell migration of L-SeMC at different concentrations (12.5,25,50,100 μmol · L-1) was detected by scratch test, the apoptosis of L-SeMC at Flow cytometry concentrations (blank, 25,50,100 μmol · L-1) was detected by Western blot, caspase 3 protein expression, SPSS 16.0 data entry and statistical analysis. Results L-SeMC inhibited the proliferation of EC9706 cells in a time-and concentration-dependent manner (P Lt; 0.001) , with 100 μmol · L -1 being the most effective. After 48 hours, the expression of apoptosis-related proteins Bax and Caspase-3 was significantly up-regulated (P Lt; 0.001) , while the expression of BCL-2 was significantly down-regulated (P Lt; 0.001) , showing a concentration-dependent change. L-SeMC had no effect on PI3K and AKT, but significantly down-regulated the phosphorylation of PI3K and Akt (P LT; 0.05) . Conclusion L-SeMC can inhibit the proliferation and induce apoptosis of EC9706 cells in a time-and concentration-dependent manner, which may be related to the inhibition of PI3K/AKT pathway.
Key words:  esophageal cancer  l-selenium-methyl Selenocysteine  apoptosiss
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