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Propofol attenuates the adhesion of tumor and endothelial cells through inhibiting glycolysis in human umbilical vein endothelial cells

查看全文 作　　者：Jie [1,2]Qi;Qichao [1,2]Wu;Xuqin [1]Zhu;Shan [3]Zhang;Xiangyuan [1,2]Chen;Wankun [1]Chen;Zhirong [1]Sun;Minmin [1]Zhu;Changhong [1]Miao 高影响力作者 机构地区：[1]Department of Anaesthesiology,Fudan University Shanghai Cancer Center,Department of Oncology,Shanghai Medical College,Fudan University,Shanghai 200032,China;[2]Department of Anaesthesiology,Shanghai Medical College,Fudan University,Shanghai 200032,China;[3]Department of Anaesthesia,Critical Care and Pain Medicine,Fudan University Shanghai Cancer Center,Department of Oncology,Shanghai Medical College,Fudan University,Shanghai 200032,China高影响力机构 出　　处：《Acta Biochimica et Biophysica Sinica》索引2019年第51卷第11期,共9页高影响力期刊 基　　金：This work was supported by the grants from the National Science Foundation of China(Nos.8187394S and 81871590);Shanghai Municipal Commission of Health and Family Planning,Key Devel oping Disciplines(No.2015ZB0104);Program of Shanghai Subject Chief Scientist(No.16XD1400900);Shanghai Shenkang Hospital Development Center Clinical Science and technology Innovation Proicct(No.SHDC12018105);the National Key R&D Program of China(No.2018YFC2001900-04);Natural Science Foundation of Shanghai(No.18ZR1407400). 摘　　要：Propofol is one of the most commonly used intravenous anesthetics and plays an important role in tumor suppression.In the present study,we aimed to investigate the mechanism by which propofol attenuates tumor endothelial cells(TECs)and tumor cell adhesion to inhibit tumor metastasis in vitro.Human umbilical vein endothelial cells(HUVECs)cultured in Dulbecco’s modified Eagle’s medium were treated with tumor conditioned medium for 24 h,followed by 4 h of treatment with or without 25μM of propofol,10μM of KN93,500μM of MK801,or 20μM of rapastinel.It was found that propofol inhibited TEC adhesion and the glycolysis level of TECs.Consistently,propofol inhibited the expressions of adhesion molecules(E-selectin,ICAM-1,and VCAM-1)and glycolysis proteins(GLUT1,HK2,and LDHA)in TECs.Moreover,propofol attenuated the expression of HIF-1α,the phosphorylation of AKT and Ca2+/calmodulin-dependent protein kinase II(CaMKII),and the Ca2+concentration in TECs.MK801,an inhibitor of NMDA receptor,and KN93,an inhibitor of CaMKII,both inhibited the expressions of adhesion molecules and glycolysis proteins,in a manner similar to propofol.Additionally,rapastine,an activator of NMDA receptor,could counteract the effects of propofol.Our results indicated that propofol attenuates intracellular Ca2+concentration,CaMKII and AKT phosphorylation,and HIF-1αexpression,probably via inhibiting the NMDA receptor,thus inhibiting glycolysis and adhesion of tumor and endothelial cells. 关 键 词：PROPOFOL TUMOR endothelial cell GLYCOLYSIS HIF-1α CAMKII RECEIVED
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