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ID:33406409
大小:4.67 MB
页数:45页
时间:2019-02-25
《沉默胃癌高尔基体α-甘露糖苷酶ⅱ(gmⅱ)对肿瘤血管生成的初步研究》由会员上传分享,免费在线阅读,更多相关内容在学术论文-天天文库。
1、重庆医科大学硕士学位论文沉默胃癌高尔基体α--甘露糖苷酶Ⅱ(GMⅡ)对肿瘤血管生成的初步研究姓名:李釩申请学位级别:硕士专业:病理学与病理生理学指导教师:易永芬201205重庆医科大学硕士研究生学位论文沉默胃癌高尔基体伐.甘露糖苷酶lI(GMI1)对肿瘤血管生成的初步研究摘要目的:初步探讨胃癌BGC.823细胞中GMII对胃癌血管形成的影响及其可能机制。方法:1.检测胃癌组织和正常胃粘膜组织中GMII的表达和CD34标记的微血管密度(MVD),分析GMII的表达和MVD之间的关系。2.采用脂质体介导法将GMII基因的真
2、核表达质粒转染入胃癌BGC.823细胞株,经G418筛选出稳定转染的细胞株。3.将胃癌BGC.823细胞与HUVEC共培养,利用RT-PCR、Westemblot,检测GMII沉默后的抑制效应以及BGC.823细胞中VEGF.A和HUVEC中VEGFR.2的表达情况。4.采取Transwell体外迁移实验方法检测GMII沉默后对共培养的HUVEC增殖,迁移的情况的影响。结果:1.1GMII蛋白分别在正常胃粘膜组织中的阳性表达率为43%(17/40);在高分化胃癌组中的阳性表达率为60%(6/lO);在中分化胃癌组中的阳
3、性表达率为59%(13/22),在低分化胃癌组织中为96%(24/25),低分化组中GMII蛋白的阳性表达率明显高于正常胃粘膜组织,差异有统计学意义(P<0.05)。1.2低分化胃癌组中MVD为(30.56士6.57)个/HP,高于正常胃粘膜组织中(23.32士7.24)个/HP,差别具有统计学意义(P4、性检测:GMII沉默组共培养的HUVEC与空白对照和空载对照组的细胞相比,增殖能力明显受抑制,差别具有统计学意义(P5、进而导致肿瘤血管生成减少,这可能与GMII基因抑制后胃癌组织中血管生成受到影响有关。关键词:GMII;VEGF.A;VEGFR.2;胃癌重庆医科大学硕士研究生学位论文EFFECTOFGMIIWER凰SILENCEDoNANGIoGENESISoFGASTRICCARCINoⅣ【AINVITRoABSTRACTobjective:ToinVestigatethee能ctofGM11weresilencedi11gast“ccancercenlinesandintheHUVECco-cuhure.T匆to6nditsmec6、hanism.Methods:1.GMIIandCD34weredetectedbyimmunohistochemicaltechlliquein40casesofnonlalgas仃icmucosaalld57casesofgastriccancertissues.TheexpressionofGMIIandCD34markersofmicrovasculardens时(MVD)wereexamindeiIlthetow铲oups,toaJlalyzetherelationshipbet、Ⅳeentheexpress7、ionGMIIandMVD.2.TheBGC-823cellswerebuildedthestableexpressionofGMIIgenethatfilteredbyG418.3.GastriccancercellsBGC-823cellsa11dHUVECco-culture.ByWestemblotandRT-PCRa11alysistoexa血netheproteinandmRNA1evelsexpressionofGMII、VEGF—Ai11gastriccancercellsandVEGFR-2inHUV8、EC.4.MigrationofHUVECwereassessedby仃answeUrnjgrationassay.Thee妇FectofGM11weresilencedonHUVECmultiplicationwasanalyzedwithMTTResults:1.GMIIproteininnomlalgastricmucosa
4、性检测:GMII沉默组共培养的HUVEC与空白对照和空载对照组的细胞相比,增殖能力明显受抑制,差别具有统计学意义(P5、进而导致肿瘤血管生成减少,这可能与GMII基因抑制后胃癌组织中血管生成受到影响有关。关键词:GMII;VEGF.A;VEGFR.2;胃癌重庆医科大学硕士研究生学位论文EFFECTOFGMIIWER凰SILENCEDoNANGIoGENESISoFGASTRICCARCINoⅣ【AINVITRoABSTRACTobjective:ToinVestigatethee能ctofGM11weresilencedi11gast“ccancercenlinesandintheHUVECco-cuhure.T匆to6nditsmec6、hanism.Methods:1.GMIIandCD34weredetectedbyimmunohistochemicaltechlliquein40casesofnonlalgas仃icmucosaalld57casesofgastriccancertissues.TheexpressionofGMIIandCD34markersofmicrovasculardens时(MVD)wereexamindeiIlthetow铲oups,toaJlalyzetherelationshipbet、Ⅳeentheexpress7、ionGMIIandMVD.2.TheBGC-823cellswerebuildedthestableexpressionofGMIIgenethatfilteredbyG418.3.GastriccancercellsBGC-823cellsa11dHUVECco-culture.ByWestemblotandRT-PCRa11alysistoexa血netheproteinandmRNA1evelsexpressionofGMII、VEGF—Ai11gastriccancercellsandVEGFR-2inHUV8、EC.4.MigrationofHUVECwereassessedby仃answeUrnjgrationassay.Thee妇FectofGM11weresilencedonHUVECmultiplicationwasanalyzedwithMTTResults:1.GMIIproteininnomlalgastricmucosa
5、进而导致肿瘤血管生成减少,这可能与GMII基因抑制后胃癌组织中血管生成受到影响有关。关键词:GMII;VEGF.A;VEGFR.2;胃癌重庆医科大学硕士研究生学位论文EFFECTOFGMIIWER凰SILENCEDoNANGIoGENESISoFGASTRICCARCINoⅣ【AINVITRoABSTRACTobjective:ToinVestigatethee能ctofGM11weresilencedi11gast“ccancercenlinesandintheHUVECco-cuhure.T匆to6nditsmec
6、hanism.Methods:1.GMIIandCD34weredetectedbyimmunohistochemicaltechlliquein40casesofnonlalgas仃icmucosaalld57casesofgastriccancertissues.TheexpressionofGMIIandCD34markersofmicrovasculardens时(MVD)wereexamindeiIlthetow铲oups,toaJlalyzetherelationshipbet、Ⅳeentheexpress
7、ionGMIIandMVD.2.TheBGC-823cellswerebuildedthestableexpressionofGMIIgenethatfilteredbyG418.3.GastriccancercellsBGC-823cellsa11dHUVECco-culture.ByWestemblotandRT-PCRa11alysistoexa血netheproteinandmRNA1evelsexpressionofGMII、VEGF—Ai11gastriccancercellsandVEGFR-2inHUV
8、EC.4.MigrationofHUVECwereassessedby仃answeUrnjgrationassay.Thee妇FectofGM11weresilencedonHUVECmultiplicationwasanalyzedwithMTTResults:1.GMIIproteininnomlalgastricmucosa
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