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1、CathepsinB、uPA和uPAR基因在肝細(xì)胞肝癌中的表達(dá)、相互關(guān)系及作用【摘要】目的:探討肝細(xì)胞肝癌(HCC)組織中組織蛋白酶B(CB)、尿激酶型纖溶酶原激活物(uPA)及其受體(uPAR)基因的表達(dá)、相互關(guān)系及作用,并分析其機(jī)制。方法:應(yīng)用RT-PCR方法測定71例肝組織標(biāo)本,包括對照組(C)12例,HCC組34例和癌旁組織(PTT)組25例的CBmRNA、uPAmRNA、uPARmRNA表達(dá),分析其間的相關(guān)性。結(jié)果:HCC組CBmRNA、uPAmRNA、uPARmRNA表達(dá)均明顯高于C組和PTT組,差異有顯著性(P<0.01),PTT組與C
2、組間差異均無顯著性(P>0.05)。CBmRNA與uPAmRNA(r=0.805),CBmRNA與uPARmRNA(r=0.786),uPAmRNA與uPARmRNA(r=0.874)之間均存在顯著的正相關(guān)關(guān)系(均P<0.01)。結(jié)論:肝癌組織CBmRNA、uPAmRNA、uPARmRNA均呈現(xiàn)高表達(dá),它們之間可能相互誘導(dǎo),協(xié)同促使肝癌的侵襲和轉(zhuǎn)移?!娟P(guān)鍵詞】癌肝細(xì)胞組織蛋白酶B尿纖溶酶原激活物尿纖溶酶原激活物受體Expression,relationshipandeffectofgeneofcathepsinB,urokinase-typep
3、lasminogenactivator(uPA)anditsreceptor(uPAR)inhepatocellularcarcinomaXUChang-long*,ZHENGJun-jie,XUEZhan-xiong,HUANGZhi-ming.*DepartmentofDigestive9Medicine,theSecondAffilatedHospitalofWenzhouMedicalCollege,Wenzhou,325027Abstract:Objective:Todeterminetheexpression,relationshipandfu
4、nctionofgeneofcathepsinB(CB),urokinase-typeplasminogenactivator(uPA)anditsreceptor(uPAR)inhepatocellularcarcinoma,andtoexploretheireffectsandmechanism.Methods:TheexpressionofCBmRNA,uPAmRNAanduPARmRNAin71specimensofhumanhepatictissue,includingcontrol(C)12,hepatocellularcarcinoma(HC
5、C)34andparatumortissueofhepatocellularcarcinoma(PTT)25weredetectedwithreversetranscription-polymerasechainraction(RT-PCR).TheexpressionofrelationshipamongCBmRNA,uPAmRNAanduPARmRNAwereresearched.Results:TheCBmRNA,uPAmRNAanduPARmRNAinHCCwereverysignificantlyhigherthanthoseinCandinPT
6、T(allP<0.01);therehadnosignificantdifferencebetweenPTTandC(allP>0.05).ThereweresignificantcorrelationbetweentheexpressionofCBmRNAanduPAmRNA(r=0.805),CBmRNAanduPARmRNA(r=0.786),uPAmRNAanduPARmRNA(r=0.874)(allP<0.01).Conclusion:TheCBmRNA,uPAmRNAanduPARmRNAshowstronglyexpres
7、sioninHCCandtheymayinduceeachother,promotecooperativelyinvasionand9metastasisofHCC.Keywords:hepatocellularcarcinoma;cathepsinB;uPA;uPAR;neoplasminvasiveness;neoplasmmetastasis基底膜和細(xì)胞外基質(zhì)是腫瘤細(xì)胞侵襲的第一道屏障。目前研究發(fā)現(xiàn),組織蛋白酶B(CathepsinB,CB)對基底膜和細(xì)胞外基質(zhì)的降解是惡性腫瘤侵襲轉(zhuǎn)移的關(guān)鍵步驟之一[1,2],尿激酶型纖溶酶原激活物(urokinas
8、e-typeplasminogenactivator,uPA)與其