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引用本文:陈伟毅,秦春宏,陈延,洪炼哲,唐峰.青藤碱通过调控PI3K/AKT通路介导的上皮间质转化抑制胰腺癌AsPC-1细胞侵袭和转移[J].中国现代应用药学,2022,39(11):1419-1425.
CHEN Weiyi,QIN Chunhong,CHEN Yan,Hong Lianzhe,TANG Feng.Sinomenine Inhibits the Invasion and Metastasis of Pancreatic Adenocarcinoma AsPC-1 Cells by Inhibiting Epithelial Mesenchymal Transition Mediated by PI3K/AKT Pathway[J].Chin J Mod Appl Pharm(中国现代应用药学),2022,39(11):1419-1425.
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青藤碱通过调控PI3K/AKT通路介导的上皮间质转化抑制胰腺癌AsPC-1细胞侵袭和转移
陈伟毅1,2, 秦春宏3, 陈延1, 洪炼哲1, 唐峰1
1.常德职业技术学院, 湖南 常德 415000;2.湖南医药学院, 湖南 怀化 418000;3.南华大学附属第二医院, 湖南 衡阳 421000
摘要:
目的 探讨青藤碱对胰腺癌AsPC-1细胞上皮间质转化(epithelial mesenchymal transition,EMT)、侵袭和转移的影响及机制。方法 采用不同浓度青藤碱作用胰腺癌AsPC-1细胞后,划痕愈合试验检测细胞愈合能力,Transwell试验检测迁移细胞数和侵袭细胞数,Western blotting检测E-cadherin、N-cadherin、Vimentin、PI3K、p-PI3K、AKT、p-AKT蛋白表达。结果 青藤碱降低AsPC-1细胞相对迁移率、迁移细胞数、侵袭细胞数。青藤碱上调E-cadherin蛋白表达、下调N-cadherin、Vimentin蛋白表达。青藤碱降低p-PI3K/PI3K、p-AKT/AKT比值。胰岛素生长因子-1逆转青藤碱对E-cadherin蛋白表达的上调和对N-cadherin、Vimentin蛋白表达的下调作用。TGF-β逆转青藤碱对AsPC-1细胞相对迁移率、迁移细胞数、侵袭细胞数的降低作用。结论 青藤碱通过调控PI3K/AKT通路介导的EMT,抑制AsPC-1细胞侵袭和转移。
关键词:  青藤碱  胰腺癌  侵袭转移  上皮间质转化  PI3K/AKT通路
DOI:10.13748/j.cnki.issn1007-7693.2022.11.005
分类号:R285.5
基金项目:湖南省教育厅科学研究项目(19C0244)
Sinomenine Inhibits the Invasion and Metastasis of Pancreatic Adenocarcinoma AsPC-1 Cells by Inhibiting Epithelial Mesenchymal Transition Mediated by PI3K/AKT Pathway
CHEN Weiyi1,2, QIN Chunhong3, CHEN Yan1, Hong Lianzhe1, TANG Feng1
1.Changde Vocational Technical College, Changde 415000, China;2.Hunan University of Medicine, Huaihua 418000, China;3.Second Affiliated Hospital of University of South China, Hengyang 421000, China
Abstract:
OBJECTIVE To find out the effect of sinomenine on epithelial mesenchymal transition(EMT), invasion and metastasis of pancreatic cancer AsPC-1 cells and related mechanisms. METHODS After treating AsPC-1 cells with different concentrations of sinomenine, the wound healing assays was used to study the healing ability of cells, the Transwell test was used to detect the number of migration and invasion of cells, the Western blotting was used to measure the expressions level of protein of E-cadherin, N-cadherin, Vimentin, PI3K, p-PI3K, AKT and p-AKT. RESULTS Sinomenine reduced the relative mobility, and the number of migration and invasion of AsPC-1 cells. Sinomenine up regulated the protein expression of E-cadherin and down regulated the protein expressions of N-cadherin and Vimentin of AsPC-1 cells. Sinomenine decreased the ratio of p-PI3K/PI3K and p-AKT/AKT. Insulin-like growth factor-1 reversed the up-regulation effect of sinomenine on E-cadherin protein expression, and down-regulation effect of sinomenine on N-cadherin and Vimentin protein expression. TGF-β reversed the decreasing effects of sinomenine on the relative mobility of AsPC-1 cells, and the number of migration and invasion of AsPC-1 cells. CONCLUSION Sinomenine inhibits invasion and metastasis of pancreatic adenocarcinoma AsPC-1 cells by inhibiting EMT mediated by PI3K/AKT pathway.
Key words:  sinomenine  pancreatic adenocarcinoma  invasion and metastasis  epithelial mesenchymal transition(EMT)  PI3K/AKT pathway
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