HAX-1对口腔鳞状细胞癌细胞的增殖和侵袭能力的作用  

Effects of HAX-1 on proliferation and invasion of oral squamous cell carcinoma cells

作　　者：孙建礼 朱青青 刘飞[1] 赵果[1] SUN Jian-li;ZHU Qing-qing;LIU Fei;ZHAO Guo(Department of oral surgery,Henan Stomatological Hospital,Zhengzhou 450000,Henan,China)

机构地区：[1]郑州大学第一附属医院、河南省口腔医院口腔外科,河南郑州450000

出　　处：《广东医学》2020年第14期1421-1426,共6页Guangdong Medical Journal

摘　　要：目的探讨HAX-1对口腔鳞状细胞癌(OSCC)细胞的增殖和侵袭能力的影响及分子机制。方法转染HAX-1 siRNA到口OSCC细胞TSCCA和Tca8223,抑制HAX-1表达;构建过表达载体pcDNA.3.1-c-Myc,转染到TSCCA和Tca8223,过表达c-Myc;AKT激动剂SC79(0、1、1.5和2μg/mL)分别孵育干扰了HAX-1的OSCC细胞24 h。免疫印迹(Western blot)检测OSCC细胞HAX-1、p-AKT和c-myc的蛋白表达量;溴脱氧尿苷(BrdU)方法检测转染后OSCC细胞的增殖能力;MTT方法检测OSCC细胞转染后的活力;transwell侵袭实验检测转染后OSCC细胞的侵袭能力。结果OSCC组织中HAX-1蛋白表达量显著升高;HAX-1 siRNA转染TSCCA和Tca8223,HAX-1、p-AKT和c-myc蛋白表达量明显降低;同时,TSCCA和Tca8223的细胞活力、增殖和侵袭能力均显著被抑制;SC79(1.5和2μg/mL)孵育干扰了HAX-1的TSCCA和Tca8223,AKT磷酸化水平和c-myc表达量明显增加。另外,转染pcDNA.3.1-c-Myc到干扰了HAX-1的TSCCA和Tca8223,c-myc蛋白表达量升高,细胞活力、增殖和侵袭能力升高。结论HAX-1可通过AKT调节c-myc的表达,进而调控OSCC细胞的增殖和侵袭的能力,为OSCC的防治提供一定的参考价值和理论基础。Objective To investigate the effects of HAX-1 on the proliferation and invasion of oral squamous cell carcinoma(OSCC)cells and its molecular mechanism.Methods HAX-1 siRNA was transfected into OSCC cells TSCCA and Tca8223 to inhibit HAX-1 expression.The overexpression vector pcDNA.3.1-c-Myc was constructed and transfected into TSCCA and Tca8223 to overexpress c-Myc.AKT agonist SC79(0,1,1.5 and 2μg/mL)was incubated with OSCC cells that interfered with HAX-1 for 24h.The protein expression levels of HAX-1,p-AKT and c-myc in OSCC cells were assessed by Western blot.The proliferation of OSCC cells after transfection was assessed using Bromodeoxyuridine(BrdU)method.The viability of OSCC cells after transfection was tested by MTT assay.The invasion ability of OSCC cells after transfection was measured by trans-well invasion assay.Results The protein expression level of HAX-1 in OSCC tissues was significantly increased.The protein expression levels of HAX-1,p-AKT and c-myc were significantly reduced after the transfection of HAX-1 siRNA in TSCCA and Tca8223.At the same time,the cell viability,proliferation and invasion abilities of TSCCA and Tca8223 were significantly inhibited.AKT phosphorylation level and c-myc expression were significantly increased following the incubation of SC79(1.5 and 2μg/mL)and HAX-1 interference in TSCCA and Tca8223,indicating that the activation of AKT could effectively block the effect of HAX-1 on c-myc expression.In addition,transfection of pcDNA.3.1-c-Myc into TSCCA and Tca8223 with HAX-1 interference increased c-myc protein expression,cell viability,proliferation and invasion abilities.Conclusion HAX-1 can regulate the expression of c-myc through AKT,thereby regulating the proliferation and invasion of OSCC cells,providing a certain reference value and theoretical basis for the prevention and treatment of OSCC.

关 键 词：口腔鳞状细胞癌 HAX-1 AKT C-MYC 

分 类 号：R739.85[医药卫生—肿瘤] R34[医药卫生—临床医学]