SOX2通过PI3K/AKT通路调控口腔鳞癌细胞迁徙的机制研究  

Mechanism of overexpression of SOX2 in regulating migration and EMT of oral squamous cell carcinoma cells through PI3K/AKT pathway

作　　者：陈昌盛 吴煜农[2] 王琪 汪长林[4] 史振怡 CHEN Chang-sheng;WU Yu-nong;WANG Qi;WANG Chang-lin;SHI Zhen-yi(De-partment of oral and milofacial surgery,Slomatological College of Nanjing Medical Unirersity,Jiangsu Nanjing 210029,China;Department of oral and mailofacial surgery,Stomatological Hospital of Jiangsu,Jiangsu Nanjing 210029,China;Department 0f Pathology,Yancheng Third People's Hospial,Jiangsu Yancheng 224001,China;Department Of Stomatology,Yancheng Third People's Hospital,Jiangsu Yancheng 224001,China.)

机构地区：[1]南京医科大学口腔医学院口腔颌面外科,江苏南京210029 [2]江苏省口腔医院口腔颌面外科,江苏南京210029 [3]盐城市第三人民医院病理科,江苏盐城224001 [4]盐城市第三人民医院口腔科,江苏盐城224001

出　　处：《临床口腔医学杂志》2021年第2期67-71,共5页Journal of Clinical Stomatology

摘　　要：目的:研究过表达SOX2通过PI3K/AKT通路促进口腔鳞癌(oral squamous cell carcinoma,OSCC)细胞迁移及上皮间质转化(epithelial mesenchymal transition,EMT)的作用及机制。方法:收集OSCC组织及正常口腔黏膜组织,培养OSCC细胞株Tca83、SCC25、HN4与正常口腔上皮细胞株FM,检测SOX2的mRNA表达水平。Tca83细胞随机分为转染阴性对照(NC)质粒的NC组、转染SOX2质粒的SOX2组、转染NC质粒并加用安慰剂的安慰剂+NC质粒组、转染SOX2质粒并加用安慰剂的安慰剂+SOX2质粒组、转染SOX2质粒并加用PI3K抑制剂LY294002的LY294002+SOX2组,检测细胞迁移、EMT标志基因波形蛋白(Vimentin)及E-钙黏蛋白(E-cadherin)、p-PI3K、p-AKT的表达量。结果:OSCC组织中SOX2的mRNA表达水平高于正常口腔黏膜组织,Tca83、SCC25、HN4细胞中SOX2的mRNA表达水平高于FM细胞且Tca83细胞中SOX2表达增加幅度最弱。与NC组比较,SOX2组Tca83细胞的迁移增强,Vimentin、p-PI3K、p-AKT的表达增加,E-cadherin的表达减少。与安慰剂+SOX2组比较,LY294002+SOX2组Tca83细胞的迁移减弱,Vimentin、p-PI3K、p-AKT的表达减少,E-cadherin的表达增加。结论:OSCC中SOX2表达增加,过表达通过激活PI3K/AKT通路促进OSCC细胞迁移及EMT。Objective:To investigate the effect and mechanism of overexpression of SOX2 on the migration and epithelial mesenchymal transition(EMT)of oral squamous cell carcinoma(OSCC)cells through PI3 K/AKT pathway.Methods:OSCC tissues and normal oral mucosa tissues were collected,OSCC cell lines Tca83,SCC25,HN4 and normal oral epithelial cell line FM were cultured,and the mRNA expression level of SOX2 was detected.Tca83 cells were randomly divided into negative control(NC)group transfected with NC plasmid,SOX2 group transfected with SOX2 plasmid,placebo+NC group transfected with NC plasmid and added with placebo,placebo+SOX2 group transfected with SOX2 plasmid and added with placebo,LY294002+SOX2 group transfected with SOX2 plasmid and added with PI3 K inhibitor LY294002.Then the cell migration,the expression of vimentin,E-cadherin,p-PI3 K and p-AKT were detected.Results:The mRNA expression of SOX2 in OSCC was higher than that in normal oral mucosa,and the mRNA expression of SOX2 in Tca83,SCC25 and HN4 cells was higher than that in FM cells,and the increase of SOX2 expression in Tca83 cells was the weakest.Compared with NC group,the migration enhanced,the expression of vimentin,p-PI3 K and p-AKT increased,and the expression of E-cadherin decreased in SOX2 group.Compared with placebo+SOX2 group,the migration weakened,the expression of vimentin,p-PI3 K and p-AKT decreased,and the expression of E-cadherin increased in LY294002+SOX2 group.Conclusion:The expression of SOX2 increases in OSCC and overexpression of SOX2 promotes migration and EMT of OSCC cells by activating PI3 K/AKT pathway.

关 键 词：口腔鳞癌 SOX2 迁移 上皮间质转化 PI3K/AKT通路 

分 类 号：R739.8[医药卫生—肿瘤]