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作 者:金家豪 赵宝生[1,2] 刘丹辉 刘玉珍[1,2,3] JIN Jia-hao;ZHAO Bao-sheng;LIU Dan-hui;LIU Yu-zhen(The First Affiliated Hospital of Xinxiang Medical University,Esophageal Cancer Institute of Xinxiang Medical University,He’nan Weihui 453100,China;Department of Thoracic Surgery,the First Affiliated Hospital of Xiniang MedicalUniversity,He’nan,Weihui 453100,China;Life ScienceResearch Center,the First Affiliated Hospital of Xinxiang Medical University,He’nan Weihui 453100,China)
机构地区:[1]新乡医学院第一附属医院新乡医学院食管癌研究所,河南卫辉453100 [2]新乡医学院第一附属医院胸外科,河南卫辉453100 [3]新乡医学院第一附属医院生命科学研究中心,河南卫辉453100
出 处:《解剖学报》2021年第2期258-263,共6页Acta Anatomica Sinica
基 金:河南省科技厅科技攻关计划项目(1152102310110);新乡医学院第一附属医院博士基金(xyyfy2014BS-002);新乡医学院研究生科研创新支持计划项目(YJSCX201914Z)。
摘 要:目的探讨低氧通过乙酰辅酶A羧化酶1(ACC1)促进人肺腺癌A549细胞迁移的机制。方法低氧(5%O2)处理肺腺癌A549细胞,应用Transwell迁移实验检测细胞迁移能力,Western blotting检测ACC1表达及上皮-间质转化(EMT)相关蛋白的表达水平。结果与常氧(对照组)相比,低氧处理促进了A549细胞的迁移(P<0.01),低氧处理后ACC1表达上调(P<0.01),同时波形蛋白(vimentin)表达增加(P<0.05),E-钙黏蛋白(Ecadherin)表达下降(P<0.01);敲除ACC1后与对照组相比,A549细胞的迁移能力减弱(P<0.05),vimentin表达下降(P<0.05),E-cadherin表达增加(P<0.01);敲除ACC1后A549细胞在常氧和5%O2条件下迁移数目及vimentin、E-cadherin表达变化无统计学意义(P>0.05);补充亚油酸(LA)恢复低氧对A549细胞的促迁移作用(P<0.05)。结论低氧通过上调ACC1的表达促进肺腺癌A549细胞迁移及EMT转化。Objective To investigate the mechanism of hypoxia to promote human lung adenocarcinoma A549 cells migration through acetyl-CoA carboxylase 1(ACC1).Methods Lung adenocarcinoma A549 cells were treated with hypoxia(5%O2).Transwell migration assay was used to detect cell migration ability.Western blotting was used to detect ACC1 expression and epithelial-mesenchymal transition(EMT)related protein expression.Results Compared with the normoxia(control group),hypoxia treatment promoted the migration of A549 cells(P<0.01),ACC1 expression was upregulated after hypoxia treatment(P<0.01),and vimentin expression was detected to increase significantly(P<0.05),Ecadherin expression decreased(P<0.01);Compared with the control group,migration of A549 cells was inhibited(P<0.05),vimentin expression was down-regulated(P<0.05),and E-cadherin expression increased after knocking down ACC1(P<0.01).After ACC1 was knocked down,the differences between the numbers of migration of A549 cells under normoxia and 5%O2 conditions and the expressions of vimentin and E-cadherin were not statistically significant(P>0.05).After linoleic acid(LA)supplementation,the hypoxia-induced migration promotion of A549 cells was restored.Conclusion Hypoxia can promote the migration and EMT transformation of lung adenocarcinoma A549 cells by up-regulating the expression of ACC1.
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