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ID:55315143
大小:1.00 MB
页数:4页
时间:2020-05-14
《肝细胞生长因子对人舌鳞癌Tca8113细胞VEGF-C表达的影响及作用机制的初步研究.pdf》由会员上传分享,免费在线阅读,更多相关内容在行业资料-天天文库。
1、·792·实用口腔医学杂志(JPractStomatol)2014Nov,30(6)肝细胞生长因子对人舌鳞癌Tca8113细胞VEGFC表达的影响及作用机制的初步研究杜洪亮何等旗张志瑞徐继莲席亚明【摘要】目的:研究HGF对人舌鳞癌Tca8113细胞中VEGFC表达的影响并探讨其作用机制。方法:体外培养Tca8113细胞,应用ELISA方法测定不同浓度HGF作用下以及分别用LY294002、U0126、SP600125、SB203580信号通路抑制剂阻断PI3K/Akt、P44/P22MAPK、JNK、P38MAPK信号通路后VEGFC的表达水平。结果:随着培养液中HGF浓度的增加,
2、Tca8113细胞中VEGFC的表达水平出现先增高后降低的趋势,当HGF浓度为40ng/ml时,VEGFC表达水平最高。PI3K/Akt信号通路抑制剂(LY294002)和P42/44MAPK信号通路抑制剂(U0126)显著抑制了HGF刺激下Tca8113的VEGFC蛋白的表达(P<0.01);而JNK信号通路抑制剂(SP600125)和P38MAPK信号通路抑制剂(SB203580)对HGF刺激下Tca8113的VEGFC蛋白的表达影响甚微(P>0.05)。结论:在人舌鳞癌Tca8113细胞中,随着HGF浓度的增加,VEGFC的表达先增高后降低。PI3K/Akt和P44/P2
3、2MAPK信号通路在口腔鳞状细胞癌淋巴转移中可能发挥作用。【关键词】口腔鳞状细胞癌;肝细胞生长因子;血管内皮生长因子C;信号通路;信号通路抑制剂TheinfluenceofHGFontheexpressionofVEGFCanditsmechanisminhumantonguesquamouscellcarcinomaTca8113cellsDUHongliang,HEDengqi,ZHANGZhirui,XUJilian,XIYaming.730000,DepartmentofOralandMaxillofacialSurgery,FirstHospitalofLanzhouUni
4、versity,China【Abstract】Objective:Toinvestigatetheinfluenceofhepatocytegrowthfactor(HGF)ontheexpressionofvascularendothelialgrowthfactorC(VEGFC)andthemechanismofHGFinducedVEGFCexpressionintonguesquamouscellcarcinomaTca8113cells.Methods:Tca8113cellswereculturedandexposedtoHGFwithvariousconcentra
5、tions.TheexpressionlevelofVEGFCwasassessedbyELISA.SignalingtransductioninhibitorsLY294002,U0126,SP600125,SB203580wasusedtoblockPI3K/Akt,P44/P22MAPK,JNK,P38MAPKsignalingpathways,respectively.Then,theexpressionlevelofVEGFCwasdetectedbyELISA.Results:TheVEGFCexpressionofTca8113cellsincreasedatthe
6、beginninganddecreasedlaterwiththeincreaseofHGFconcentration.WhentheconcentrationofHGFwas40ng/ml,VEGFCexpressionlevelwasthehighest.InhibitorLY294002ofPI3K/AktandInhibitorU0126ofP44/P22MAPKsignificantlyblockedtheeffectsonHGFinducedVEGFCupregulation(P<0.01).InhibitorSP600125ofJNKandinhibitorSB2
7、03580ofP38MAPKdidn'tinterfereHGFinducedVEGFCexpression(P>0.05).Conclusion:HGFcontributedtotheexpressionofVEGFC,PI3K/AktandP44/P22MAPKsignalingpathwaysmaybeinvolvedinHGFinducedVEGFCupregulation,andmayplaypotential
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