Pannexin1通道对乳腺癌细胞MCF-7细胞增殖和侵袭迁移的影响及可能机制  

Effect of Pannexin1 Channel on Proliferation and Migration in Breast Cancer Cell MCF-7 and Its Mechanism

作　　者：宋炬东 丁云贞 张超 孙远远 刘号峰 SONG Ju-dong;DING Yun-zheng;ZHANG-Chao;SUN Yuan-Yuan;LIU Hao-feng(People’s Hospital of Lin'an District,Hangzhou 311300 China;Bengbu Medical College of Anhui Province,Bengbu 233000,China;First People’s Hospital of Suzhou City,Anhui Province,Suzhou 234000,China)

机构地区：[1]杭州市临安区人民医院,浙江杭州311300 [2]蚌埠医学院,安徽蚌埠233000 [3]宿州市第一人民医院药剂科,安徽宿州234000

出　　处：《肿瘤学杂志》2020年第3期210-215,共6页Journal of Chinese Oncology

摘　　要：[目的]探究Pannexin1对乳腺癌细胞MCF-7增殖、侵袭迁移的影响及可能机制。[方法]MTT法检测0、12.5、25、50、100、200μmol/L甘珀酸(CBX)对乳腺癌细胞MCF-7增殖能力的影响;集落克隆检测CBX对乳腺癌细胞MCF-7增殖能力的影响;采用实时荧光法检测细胞间荧光传递能力;化学发光法检测细胞外ATP浓度。使用100μmol/LCBX处理乳腺癌细胞MCF-7后,Transwell法检测MCF-7细胞的侵袭迁移能力;Western印迹法检测乳腺癌细胞中相关蛋白p-ERK1/2、ERK1/2、Vimentin、MMP-9蛋白的表达。[结果]MTT实验结果表明,200μmol/L CBX可显著性抑制MCF-7细胞增殖能力(P<0.05),而100μmol/L CBX对MCF-7细胞增殖能力无显著性抑制作用(P>0.05)。集落克隆实验结果表明,200μmol/L CBX可显著性抑制MCF-7细胞增殖能力(P<0.05)。实时荧光法和化学发光法实验结果表明,100μmol/L和200μmol/L CBX显著性抑制Pannexin1通道功能(P<0.05);Transwell实验和划痕实验结果表明,100μmol/L CBX显著性抑制乳腺癌MCF-7细胞侵袭迁移能力(P<0.05);Western印迹法结果表明,CBX抑制Pannexin1后,乳腺癌细胞MCF-7中ERK1/2、p-ERK1/2、MMP-9和Vimentin蛋白表达量下降(P<0.05)。[结论]200μmol/L CBX抑制Pannexin1通道后,乳腺癌MCF-7细胞活性和增殖能力减弱,而100μmol/L CBX可降低乳腺癌MCF-7细胞侵袭迁移能力,其机制可能与ERK1/2表达量下降有关。[Objective]To investigate the effect and mechanism of pannexin1(Panx-1)channel on proliferation,invasion and migration of breast cancer MCF-7 cells.[Methods]Breast cancer MCF-7 cells were treated with different concentrations of Panx-1 channel inhibitor carbenoxolone(CBX)(0,12.5,25,50,100,200μmol/L).Cell proliferation was detected by MTT assay and colony cloning assay.The intercellular fluorescence transmission ability was detected by real-time fluorescence assay,and the extracellular ATP concentration was measured by chemiluminescence assay.Transwell method was used to detect the invasion and migration ability of MCF-7 cells.Western blotting was used to detect the expression of Panx-1 channel related proteins p-ERK1/2,ERK1/2,vimentin and MMP-9 in breast cancer cells.[Results]MTT assay showed that 200μmol/L CBX significantly inhibited the viability of MCF-7 cells(P<0.05),while 100μmol/L CBX had no significant inhibitory effect on MCF-7 cells(P>0.05).The results of colony cloning experiments showed that 200μmol/L CBX significantly inhibited the proliferation of MCF-7 cells(P<0.05),while 100μmol/L CBX had no significant inhibitory effect on MCF-7 cells(P>0.05).Real-time fluorescence and chemiluminescence experiments showed that 100μmol/L and 200μmol/L CBX significantly inhibited pannexin1 channel function(P<0.05).Transwell assay and scratch test results showed that 100μmol/L CBX significantly inhibited the invasion and migration ability of MCF-7 cells(P<0.05).Western blotting results showed that the expression of ERK1/2,p-ERK1/2,MMP-9 and Vimentin in breast cancer MCF-7 cells was decreased after CBX treatment(P<0.05).[Conclusion]Inhibiting pannexin1 channel by 200μmol/L CBX,the viability and proliferation of breast cancer MCF-7 cells are decreased,while 100μmol/L CBX can reduce the invasion and migration ability of breast cancer MCF-7 cells,which may be related to the expression of ERK1/2 proteins.

关 键 词：乳腺癌 Pannexin1 增殖 侵袭 迁移 

分 类 号：R737.9[医药卫生—肿瘤]