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黄连素抗食管癌EC109细胞的作用及其机制

刘红岗 闫小龙 赖远阳 朱以芳 同李平 董小平 许娟 张勇 郭海华 李小飞

国际病理科学与临床杂志2017,Vol.37Issue(12):2524-2529,6.
国际病理科学与临床杂志2017,Vol.37Issue(12):2524-2529,6.DOI:10.3978/j.issn.2095-6959.2017.12.002

黄连素抗食管癌EC109细胞的作用及其机制

Inhibition of berberine on ECI09 cells in esophageal cancer and its machanism

刘红岗 1闫小龙 1赖远阳 1朱以芳 1同李平 1董小平 1许娟 1张勇 1郭海华 1李小飞1

作者信息

  • 1. 第四军医大学唐都医院胸外科,西安710038
  • 折叠

摘要

Abstract

Objective:To investigate the role ofberberine (BBR) on esophageal cancer and its mechanism.Methods:EC109 cells were treated with 50,100,200 μmol/L BBR and the CCK8 assay and cell migration assay were conducted.Further,we detected the phosphorylation level of Akt,the location of FOXO3,B-cell lymphoma-2 (bcl-2) and Bax expression through Western blot.To further evaluate whether BBR has an anti-tumor growth effect in vivo,we measured the tumor volume in a tumor bearing model by transplanting EC109 cells into nude mice.Results:After treated by BBR,EC109 cell viability was significantly reduced compared with the control group (P<0.05).Distance between cell boundary was significantly increased,indicating a worse migration ability (P<0.05).Compared with the control group,pAkt expression/total Akt expression was significantly decreased after BBR treatment.Cytoplasmic FOXO3 decreased and nucleus FOXO3 increased.Bcl-2 was decreased and Bax was increased by BBR.In vivo study showd that tumor volumes in nude mice were significantly reduced after BBR treatment.Conclusion:BBR can inhibit EC109 cell growth and induce cell apoptosis,which might be mediated by regulation of Akt/FOXO3 pathway.

关键词

黄连素/食管癌/蛋白激酶B/叉头蛋白转录因子3/细胞核转位/细胞凋亡

Key words

berberine/esophageal cancer/Akt/forkhead box O3/nuclear translocation/cell apoptosis

引用本文复制引用

刘红岗,闫小龙,赖远阳,朱以芳,同李平,董小平,许娟,张勇,郭海华,李小飞..黄连素抗食管癌EC109细胞的作用及其机制[J].国际病理科学与临床杂志,2017,37(12):2524-2529,6.

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