简介:摘要:目的 探讨E-cadherin及P-cadherin蛋白在甲状腺乳头状癌组织中的表达情况及临床意义。方法 采用免疫组化法检测E-cadherin及P-cadherin蛋白在甲状腺乳头状癌组织及癌旁正常组织中的表达,并分析二者的表达与临床病例特征的相关性。结果 相对于癌旁正常组织,E-cadherin蛋白在甲状腺乳头状癌组织中的表达率降低,二者的表达率分别为100.0%和20.0%(P<0.000),而P-cadherin蛋白在甲状腺乳头状癌组织中表达增加,二者的表达率分别为15.0%,和77.5% (P<0.000)。甲状腺乳头状癌组织中E-cadherin蛋白的表达与肿瘤包膜侵袭、淋巴结转移及肿瘤TNM分期密切相关(P<0.05),而与性别、年龄及肿瘤大小等临床病理特征无明显相关(P>0.05);甲状腺乳头状癌组织中P-cadherin蛋白的表达仅与淋巴结转移及肿瘤TNM分期相关(P<0.05),与其他临床病理特征无明显相关性(P>0.05)。结论E-cadherin、P-cadherin蛋白的异常表达可能在甲状腺乳头状癌的发生、浸润及转移过程中发挥重要作用。
简介:摘要目的探讨甲状腺乳头状癌患者血清P-钙粘蛋白(P-Cadherin)、细胞角蛋白-19(CK-19)和基质金属蛋白酶-9(MMP-9)的变化,以及甲状腺切除术后131I治疗对其的影响。方法对50例甲状腺乳头状癌患者采用甲状腺全切术,术后1个月行131I核素治疗,1个月后测定患者治疗前后血清中P-Cadherin、CK-19和MMP-9水平。结果甲状腺乳头状癌组血清P-Cadherin、CK-19和MMP-9水平较对照组显著升高(P<0.01),且甲状腺乳头状癌伴淋巴结转移患者比无伴淋巴结转移患者血P-Cadherin、CK-19和MMP-9水平显著升高(均P<0.01);甲状腺乳头状癌患者不伴淋巴结转移组和伴淋巴结转移组患者行甲状腺切除术后131I治疗后血清P-Cadherin、CK-19和MMP-9的含量较治疗前均降低(均P>0.05);且伴淋巴结转移组治疗后血清P-Cadherin、CK-19和MMP-9的含量较不伴淋巴结转移组降低更显著(均P<0.01)。结论血清P-Cadherin、CK-19和MMP-9可能与甲状腺乳头状癌发生发展有关,甲状腺切除术后131I治疗能显著降低甲状腺乳头状癌患者P-Cadherin、CK-19和MMP-9水平,以期达到早期诊断早期防治的目的。
简介:目的探讨脊柱脊索瘤中E-cadherin和P120ctn的表达及其与肿瘤临床病理特征、肿瘤局部复发之间的关系。方法应用免疫组化方法检测40例脊柱脊索瘤标本和5例胎儿脊索组织标本中E-cadherin和P120ctn的表达情况。结果脊索瘤标本中E-cadherin和P120ctn的胞膜表达减低率分别为75.0%(30例)和67.5%(21例)。E-cadherin的表达与肿瘤侵犯的椎节数目之间存在相关性(P〈0.05),P120ctn的表达与肿瘤的病理学分级存在相关性(P〈0.01)。二者均与肿瘤的平均复发时间之间存在相关性(P〈0.05和P〈0.01)。另外,E-cadherin和P120ctn的表达下调之间存在相关性(P〈0.05)。COX回归模型分析证实P120ctn和肿瘤病理分级是脊柱脊索瘤术后局部复发的独立预测因素。结论脊柱脊索瘤中常发生E-cadherin和P120ctn的胞膜表达下调,且与脊柱脊索瘤的发生、发展有关。二者均是肿瘤侵袭和局部复发的有价值的生物学预测指标,P120ctn是脊柱脊索瘤局部复发的独立预测因素。
简介:ObjectiveToinvestigatethehypermethylationstatusofglutathionetransferaseP1(GSTP1)andE-cadherin(ECAD),TSGs(tumorsuppressorgenes)inourbreastcancersamplesandexploretheircorrelationwithclinicopathologicalfeaturesofcorrespondingcancerpatients.MethodsOnehundredandthirty-sixIDC(invasiveductalcarcinoma)patientswererecruitedforanalysisand16fibroadenomapatientsactedascontrol.DNAextractionandmethylation-specificPCR(MSP)weresubsequentlyperformedprecededbypathologicalexamination.ResultsThepercentageofhypermethylatedGSTP1incarcinomaandfibroadenomagroupswas34.92%and15.79%respectivelyandthepercentageofhypermethylatedECADincarcinomasandfibroadenomaswas18.00%and0.00%respectively.Carcinomahadthehighestpercentageofc-erbB2overexpressionbeing54.55%amongtheclinicopathologicalparameters.ConclusionHypermethylationpatternsarefrequentinIDCandseemtorelatetoc-erbB2overexpression,andsuchepigeneticchangeshouldnotbeneglectedinfibroadenoma.Tumormethylationstatusincancerpatientscanbedeterminedatearlystageanditmaybeareferenceforbettertreatmentplanning.
简介:目的探讨神经-钙粘素(N—cadherin),上皮-钙粘素(E—cadherin)及B—catenin在人脑胶质瘤中的表达及意义。方法采用S—P免疫组化方法检测N—cadherin、E—cadherin、β—catenin在42例不同级别胶质瘤及8例正常脑组织中的表达。结果N—cadherin,E—cadherin及β—catenin的表达在正常脑组织与胶质瘤之间以及胶质瘤的高低级别组间存在显著差异(P〈0.05),并且在生存时间〉2年组与生存时间≤2年组间差别显著(P〈0.05);N—cadherin与β—catenin的表达随着肿瘤级别的升高而增高,且二者在胶质瘤中的表达呈正相关(P〈0.05,r=0.778)。E—cadherin的表达随着肿瘤级别的升高而下降,E—cadherin与N—cadherin、β—catenin的表达呈负相关(P〈0.05,r1=-0.747,r2=-0.783);结论提示N—cadherin与β—catenin的过度表达和E—cadherin的表达下调在胶质瘤的侵袭及恶性进展中起着重要作用。N—cadherin与β—catenin的表达可能与胶质瘤患者的预后密切相关,提示可作为反映胶质瘤恶性程度与预后的指标。
简介:AbstractImportance:Cadherin-11 (CDH11), a cell-to-cell adhesion molecule, is implicated in the fibrotic process of several organs. Biliary atresia (BA) is a common cholestatic liver disease featuring cholestasis and progressive liver fibrosis in children. Cholestatic liver fibrosis may progress to liver cirrhosis and lacks effective therapeutic strategies. Currently, the role of CDH11 in cholestatic liver fibrosis remains unclear.Objective:This study aimed to explore the functions of CDH11 in cholestatic liver fibrosis.Methods:The expression of CDH11 in BA livers was evaluated by database analysis and immunostaining. Seven BA liver samples were used for immunostaining. The wild type (Wt) and CDH11 knockout (CDH11-/-) mice were subjected to bile duct ligation (BDL) to induce cholestatic liver fibrosis. The serum biochemical analysis, liver histology, and western blotting were used to assess the extent of liver injury and fibrosis as well as activation of transforming growth factor-β (TGF-β)/Smad pathway. The effect of CDH11 on the activation of hepatic stellate cell line LX-2 cells was investigated.Results:Analysis of public RNA-seq datasets showed that CDH11 expression levels were significantly increased in livers of BA, and CDH11 was correlated with liver fibrosis in BA. BDL-induced liver injury and liver fibrosis were attenuated in CDH11-/- mice compared to Wt mice. The protein expression levels of phosphorylated Smad2/3 were decreased in livers of CDH11-/- BDL mice compared to Wt BDL mice. CDH11 knockdown inhibited the activation of LX-2 cells.Interpretation:CDH11 plays an important role in cholestatic liver fibrosis and may represent a potential therapeutic target for cholestatic liver disease, such as BA.
简介:Thestiffnessandstrengthofextracellular(EC)regionofcadherinareproposedtobetwoimportantmechanicalpropertiesbothforcadherinasamechanotransductorandfortheformationofcell-celladhesion.Inthisstudy,wequantitativelycharacterizedthestiffnessandstrengthofECstructurewhenitbindswithdifferenttypesofionsbymoleculardynamicssimulations.ResultsshowthatECstructureexhibitsarod-likeshapewithhighstiffnessandstrengthwhenitbindswiththebivalentionsofcalciumormagnesium.However,itswitchestoasoftandcollapsedconformationwhenitbindswiththemonovalentionsofsodiumorpotassium.ThisstudyshedslightontheimportantroleofthebivalentionsofcalciuminthephysiologicalfunctionofEC.
简介:目的研究富含亮氨酸重复序列免疫球蛋白样蛋白1(LRIG1)、表皮生长因子受体(EGFR)、ECadherin及N-Cadherin在不同病理级别胶质瘤中表达差异,探讨LRIG1在胶质瘤恶性进展中可能的作用机制。方法收集74例胶质瘤患者手术标本,包含12对原发及复发配对胶质瘤标本,采用qRT-PCR检测LRIG1、EGFR、E-Cadherin、N-Cadherin基因的表达,并采用免疫印迹检测LRIG1、EGFR、E-Cadherin、NCadherin、Vimentin蛋白表达情况。结果随着胶质瘤病理级别的升高,LRIG1、E-Cadherin基因及蛋白表达水平降低,EGFR、N-Cadherin基因及蛋白表达水平升高,差异均具有统计学意义(均P〈0.05)。WHOⅢ-Ⅳ组胶质瘤EGFR/LRIG1及N-Cadherin/E-Cadherin比值显著高于WHOⅠ-Ⅱ组(均P〈0.05)。EGFR/LRIG1与NCadherin/E-Cadherin变化之间存在正相关(r=0.56,P〈0.05)。对原发及复发配对胶质瘤标本的研究结果与上述一致。结论胶质瘤中EGFR/LRIG1表达失衡,可能通过诱导上皮间质转化(EMT)促进胶质瘤细胞的恶性进展。LRIG1可能成为胶质瘤治疗的新靶点。
简介:摘要目的探讨P73、nm23H1、E-cadherin基因在胃癌组织中的临床意义及其相关性研究。方法采用免疫组化SP法检测160例胃癌标本中P73、nm23H1、E-cadherin的表达。结果胃癌组织中P73、nm23H1、E-cadherin的阳性表达率分别为51.7%、61.5%、82.1%,均低于相应癌旁正常组织93.6%、94.5%、97.1%(P<0.05)。P73、nm23H1、E-cadherin表达与肿瘤分化程度、浸润深度、淋巴结转移有关,P73表达的胃癌病人预后差,nm23H1、E-cadherin表达的胃癌病人预后好。结论P73、nm23H1、E-cadherin基因表达与胃癌发生、发展、侵袭和转移有关。nm23H1、E-cadherin表达对胃癌的转移可能有协同作用。
简介:瞄准:在人的肝细胞癌(HCC)检验E-cadherin的免疫反应和catenin家庭的四种子类型并且调查在HCC病人的E-cadherin/catenin复杂、临床病理的参数的表示之间的关联。方法:免疫为E-cadherin和catenins的组织化学的学习在HCC的97个修理福尔马林的、嵌入石蜡的标本上被执行。结果:E-cadherin的减少的表示,alpha-,贝它--,gamma-catenin和p120分别地在69%,76%,63%,71%和73%被观察。E-cadherin和catenin部件的两表示显著地与肿瘤等级被相关(P=0.000)。它显示出在catenin成员和肿瘤舞台的表示之间的有效差量(P=0.003,P=0.017,P=0.007并且P=0.000,分别地)。在HCC的E-cadherin的减少的表示显著地与肝内转移(IM)和胶囊的侵略被相关(P=0.008,P=0.03,分别地)。靠近的关联也在catenins和肿瘤尺寸的表示之间被观察(P=0.002,P=0.034,P=0.016并且P=0.000,分别地)。另外,每catenin的表示被发现与IM相关(P=0.012,P=0.049,P=0.026并且P=0.014,分别地)。不,统计上,有效差量在E-cadherin/catenin建筑群和淋巴节点允许的表达式水平之间被观察,脉管的侵略和卫星小瘤。有趣地,仅仅p120的表示与法新社价值显示出关联(P=0.035)。E-cadherin的表示与alpha-一致,贝它--,gamma-catenin和p120表示(P=0.000)。最后,E-cadherin/catenin建筑群的反常表示显著地与病人的幸存被联系(P=0.0253,P=0.0052,P=0.003,P=0.0105并且P=0.0016,分别地)。不过,E-cadherin/catenin建筑群的部件都不是HCC病人的独立预示的因素。结论:E-cadherin,catenins和p120的下面调整的表达式在HCC经常发生并且贡献肿瘤的前进和开发。检测复杂的E-cadherin/catenin的合作表示可以比在预言肿瘤侵略,转移和病人是幸存探索他们之一是准确、珍贵的更多。
简介:NUK儿童安全牙膏德国品质无氟温和配方,有效保护宝宝牙龈与牙齿本品为婴幼儿专用配方,不含氟、刺激性SLS、麸质、糖和人工甜昧剂,温和无刺激。保护宝宝萌出的第一颗小乳牙,温和清洁宝宝口腔。含木糖醇和维生素E,有效营养牙龈并预防蛀牙,清新的苹果香蕉味,让宝宝不抗拒刷牙。德国制造,原装进口,符合欧盟与国标标准。经典升级非同以往植村秀全新如胶似漆眼线笔2013年.植村秀推出第一款具有划时代意义的笔状眼线胶.并以其柔滑如胶、浓郁似漆的特点在眼线市场上拔得头筹。2017年。如胶似漆
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简介:目的研究E-cad在食管鳞状细胞癌中的表达及意义。方法免疫组化SABC法检测76例食管癌E-cad的表达。结果正常食管粘膜细胞膜E-cad表达呈阳性。在癌组织中,E-cad细胞膜表达减弱。E-cad减弱表达率为65.8%(50/76),E-cad表达与病理分化程度(P=0.02)、漫润深度(P=0.024)、静脉侵犯(P=0.04)、淋巴结转移(P=0.022)和临床分期(P=0.04)具有相关性;而与年龄、性别、病理类型无关(P>0.05)。在无淋巴结转移组E-cad表达降低占56.25%(27/48),有淋巴结转移组占82.14%(23/28),两者之间表达差异有显著性;有静脉侵犯组E-cad表达降低率为92.86%(13/14)和无静脉侵犯组为59.68%(37/62),两者之间差异有显著性。结论E-cad减弱表达与食管癌生物学行为有关,可能为食管癌预后差的因素之一。
简介:AIM:Toexploretheeffectsandmechanismofvascularendothelialcadherin(VE-cadherin)onexperimentalcornealneovascularization(CRNV).·METHODS:MousecorneaswereburnedwithsodiumhydroxidetobuildaCRNVmodel.Theburnedcorneaswerelocallyadministratedwithanti-mouseVE-cadherinneutralizingantibody.AnnexinVandclusterofdifferentiation31(CD31)doublestainingwasusedtomeasurevascularendothelialcellapoptosiswiththeuseofflowcytometry(FCM).TheproteinexpressionofNADPHoxidase2(Nox2),caspase-3,andproteinkinaseC(PKC)intheburnedcorneaswereexaminedbyWesternblot.Humanretinalendothelialcell(HREC)proliferationwasdetectedusingaCellCountingKit8(CCK-8)assayinvitro.·RESULTS:TheamountofCRNVpeakedtwoweeksafterthealkaliburn.FCMconfirmedthatVE-cadherinneutralizingantibodytreatmentincreasedCD31positivecellapoptosis.WesternblotrevealedthattheintracornealproteinexpressionofNox2andcaspase-3wereup-regulated,whilePKCwasdown-regulatedintheVE-cadherinneutralizingantibodyadministratedgroup.CCK-8assayshowedthatVE-cadherinneutralizingantibodymarkedlyinhibitedHRECproliferation.·CONCLUSION:VE-cadherinexhibitedananti-apoptosiseffectthroughenhancedPKCsignalingandanenhancedcellproliferationpathway.
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