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| 1 | 肝癌细胞β-catenin表达及其亚细胞内分布显示文摘目的肝癌细胞在细胞膜、细胞浆和细胞核β-catenin蛋白分布及其与肝癌分化程度的关系。方法利用免疫组织化学和Western Blotting两种方法检测正常肝、肝硬化和肝癌组织细胞表达pcatenin,及其在细胞膜、细胞浆和细胞核内分布情况。结果正常肝、肝硬化细胞膜β-catenin分布均匀、清晰、完整,细胞浆仅有少许黄色颗粒,Western Blotting显示胞浆及胞核无明显β-catenin分布。免疫组化显示肝癌细胞膜β-catenin分布不均匀、不连续,甚至缺如,低分化肝癌细胞膜β-catenin分布较高分化癌少,肝癌细胞浆呈现β-catenin高表达。18例(90%)肝癌细胞膜β-catenin表达量明显减少,10例(50%)胞膜分布不连续或缺如,细胞间界限不清楚,癌细胞大小也不一致;17例(85%)细胞浆明显的pcatenin积聚,而且细胞浆分布不均匀;随肝癌分化程度不同,pcatenin表达也有明显差异,7例(77.8%)高分化肝癌细胞膜pcatenin分布较为清楚连续,细胞间有界限,细胞浆表达量较多,分布均匀。4例(80%)低分化肝癌pcatenin细胞膜表达较少细胞界限不清楚,细胞浆pcatenin分布不均匀,呈点状积聚。中度分化的肝癌细胞膜和细胞浆内pcatenin分布界与高低分化之间,5例(83.3%)细胞浆pcatenin表达阳性。Western Blotting检测肝癌细胞浆和细胞核均有分布,且核内积聚免疫组化法难以观察。结论肝癌细胞pcatenin表达在细胞膜、细胞浆和胞核异常分布与Wnt信号细胞内转导异常,这可能与肝癌快速增殖、高侵袭和转移有关,为肝癌的临床治疗和新药研究提供了理论基础。 | 金世龙 刘宏鸣 刘宝华 杨俊涛 顾红光 申海军 肖静 | 2007 | 中华肝胆外科杂志2007，13，9： | 8 |
| 2 | 经典的Wnt信号通路在大鼠肝脏卵圆细胞增殖和分化中的作用显示文摘目的探讨激活经典的Wnt信号转导通路在大鼠肝脏卵圆细胞增殖、分化中的作用。方法不同浓度的重组Wnt3a纯化蛋白(20,40,80,160,200ng/ml)在无血清培养条件下作用WB-F344细胞24h,Brdu掺入法检测细胞增殖情况。160ng/ml重组Wnt3a纯化蛋白在无血清条件下作用WB-F344细胞,作用24h后通过免疫荧光观察β-catenin亚细胞定位的变化,Western-blot观察β-catenin蛋白表达的变化;半定量RT-PCR观察下游靶基因CyclinD1mRNA表达的变化。作用72h后通过RT-PCR观察CK-19,AFP,ALB,HNF-6,HNF-4αmRNA表达的变化,Western-blot观察CK-19,AFP蛋白表达的变化。以同期未做处理的WB-F344细胞作为空白对照。结果不同浓度的重组Wnt3a纯化蛋白作用后,处理组WB-F344细胞以剂量依赖方式增殖,Wnt3a处理组明显高于空白对照组(P<0.05),160ng/ml作用时,增殖达到最高峰。Wnt3a(160ng/ml)作用24h后,通过免疫荧光共聚焦观察β-catenin的亚细胞定位发现,处理组β-catenin在WB-F344主要在细胞核中表达;而未处理组主要在核周表达;Western-blot发现处理组β-catenin蛋白表达轻度增加;半定量RT-PCR发现下游靶基因CyclinD1mRNA的表达显著增加(P<0.01)。72h后,RT-PCR发现两组中均有AFP,CK-19,HNF-6,HNF-4α基因表达,而ALB在两组中均不表达;同时通过Western-blot发现AFP,CK-19蛋白在两组中均有表达。结论激活经典的Wnt信号转导通路促进大鼠肝脏卵圆细胞系WB-F344的增殖和自我更新。 | 张影 綦盛麟 程宁 张勇 | 2011 | 中华临床医师杂志(电子版)2011，5，15： | 4 |
| 3 | β-catenin和TGF-β1在原发性肝癌中的表达及临床意义显示文摘目的探讨β-catenin和TGF-β1在原发性肝癌(Hepatocellular carcinoma,PHC)中的表达及与临床病理参数的关系。方法采用非生物素二步免疫组化方法检测45例PHC癌组织及相应癌旁组织中β-catenin和TGF-β1的表达情况。结果β-catenin在肝癌组织、癌旁组织中的阳性率分别为51.1%、26.7%,两者之间差异有统计学意义(P<0.05);TGF-β1在肝癌组织、癌旁组织中的阳性率分别为40%、20%,两者之间差异亦有统计学意义(P<0.05);β-catenin和TGF-β1的异常表达均与表面抗原(HBsAg)、门脉癌栓、淋巴结转移和包膜相关(对应χ2值和P值分别为4.980、0.026;3.972、0.046;6.622、0.040;9.738、0.002和3.534、0.060;5.526、0.019;10.385,0.001;9.142、0.002);β-catenin和TGF-β1表达存在相关关系(P<0.05)。结论β-catenin、TGF-β1在PHC中的表达可能协同促进了PHC的发生、发展。 | 赵伟 李昭宇 | 2011 | 宁夏医科大学学报2011，33，10： | 3 |
| 4 | β-catenin在肝癌组织中的表达及对肝癌患者预后的影响显示文摘目的:探讨β-catenin在肝细胞癌(HCC)组织中的表达及其与肝癌预后的关系。方法:用免疫组织化学方法检测83例HCC、26例癌旁组织和5例正常肝组织中β-catenin蛋白的表达情况,并对行肝癌根治性术患者进行术后随访,分析β-catenin蛋白表达与临床因素、HCC病理分化程度及患者术后生存的关系。结果:β-catenin蛋白在HCC、癌旁组织及正常肝组织中的阳性表达率分别为68.67%(57/83)、30.77%(8/26)和20%(1/5),其在HCC中的表达阳性率高于正常肝组织及癌旁组织(P<0.05);β-catenin阳性表达率与肝癌病理分化程度呈负相关(r=-0.34,P=0.027);有效随访68例,在随访的5年内,β-catenin阳性表达组平均生存时间11.2个月,β-catenin阴性表达组平均生存时间26.6个月,Kaplan-Meier生存分析表明β-catenin阴性表达患者比阳性表达患者术后生存更长,Log-Rank检验两组预后有显著性差异(χ~2=15.138,P=0.000)。结论:β-catenin与HCC分化程度相关,β-catenin在肝癌组织中的高表达提示患者预后不良。 | 刘德忠 常波 林飞翔 李学东 | 2017 | 癌变.畸变.突变2017，29，4： | 3 |
| 5 | siRNA对肝癌HepG2细胞β-catenin表达和细胞增殖的抑制作用显示文摘目的研究siRNA对肝癌HepG2细胞β-catenin基因表达,β-catenin蛋白翻译及细胞增殖的抑制作用。方法利用RT—PCR检测β-eatenin基因表达,Western Blotting方法检测肝癌HepG2细胞株β-eatenin表达和HepG2细胞增殖曲线的变化。结果shRNA转染后1dA和B组β-catenin表达弱于C和D组,2dA和B组pcatenin表达更弱,3d几乎未见表达。A和B组间比较无显著差异(P〉0.05),A,B与C、D组比较相差非常显著(P〈0.01)。A,B两处理组细胞转染后每天所检测抑制率均显著高于对照组(P〈0.01),表明细胞经A、B处理后生长受到明显抑制;两处理组细胞生长抑制率5d内逐渐增高。A与B和C与D组间差异无统计学意义(P〉0.05)。加入siRNA的两实验组(A,B组)β-catenin蛋白表达明显较少,对照C,D组β-catenin蛋白表达较多,提示siRNA抑制了HepG2细胞的β-catenln蛋白表达。结论针对β-eatenin的shRNA能够抑制β-cateninmRNA表达,使胞浆中的β-cateninmRNA下降,细胞β-catenin蛋白表达明显减少,HepG2细胞增殖受到明显的抑制.这种作用对临床肿瘤有潜在的治疗价值。 | 金世龙 谢斌 刘宏鸣 顾红光 刘宝华 | 2009 | 中华肝胆外科杂志2009，15，12： | 3 |
| 6 | 乙型肝炎病毒及黄曲霉毒素暴露的肝细胞癌中β-catenin、PTEN的mRNA表达显示文摘目的研究β-catenin、PTEN基因在乙型肝炎病毒(HBV)及黄曲霉毒素B1(AFB1)暴露下肝细胞癌(HCC)中mRNA表达,探讨在双暴露情况下β-catenin、PTEN与HCC发生、发展的关系。方法根据HBV与AFB1的暴露情况,将108例肝细胞癌手术切除研究对象分为4组,A组:HBV(+)/AFB1(+)48例;B组:HBV(+)/AFB1(-)27例;C组:HBV(-)/AFB1(+)19例;D组:HBV(-)/AFB1(-)14例。同时收集正常肝组织者20例,分别来自肝外伤、肝血管瘤、肝移植供体等手术切除标本作为正常对照组。采用逆转录-PCR(RT-PCR)法检测β-catenin基因与PTEN基因的mRNA表达情况,分别对各组的表达情况进行比较。结果 RT-PCR显示,β-catenin基因mRNA的半定量平均灰度值A组(1.13±0.14)、C组(1.16±0.18)分别与D组(1.01±0.13)相比,差异有统计学意义(P<0.05),此外,A、B(1.06±0.18)、C、D组与正常对照组比较,差异均有统计学意义(P<0.001)。PTEN基因mRNA的半定量平均灰度值A组(0.54±0.13)、B组(0.59±0.16)分别与C组(0.97±0.16)及D组(0.92±0.13)相比,差异有统计学意义(P<0.05)。此外,A、B、D组与正常对照组相比,差异有统计学意义(P<0.05)。结论β-catenin基因的高表达率可能与AFB1高暴露有关,PTEN基因的失活与HBV高感染率有关。 | 陈德凤 齐鲁楠 彭涛 罗国容 黎乐群 | 2014 | 重庆医学2014，43，14： | 2 |
| 7 | Role of β-catenin in hepatocarcinogenesis of rats显示文摘BACKGROUND: β-catenin has two distinct roles in E-cadherin mediated cell adhesion and carcinogenesis by activating the wnt/β-catenin signaling pathway. One occurs at the cell-adhesion site, where cadherins are linked to the actin-based cytoskeleton. The other takes place in the cytoplasm and nuclei and is thought to regulate cell transformation. We studied the role of β-catenin in hepatocarcinogenesis of rats. METHODS: Fresh liver specimens were obtained from normal rats. and atypical hyperplasia livers and hepatocarcinoma tissues from model rats. The changes of β-catenin in gene expression levels were detected by reverse transcriptase polymerase chain reaction (RT-PCR) in the different specimens separately. At the same time, their localization was observed immunohistochemically. RESULTS: In the normal liver specimens, β-catenin staining was seen in the cell membrane. In liver specimens of atypical byperplasia, β-catenin staining occurred in the cell cytoplasm of some cells as well as in the cell membrane of others. Immunohistochemically cancerous tissues showed the presence of β-catenin in the cytoplasm and nuclei. RTPCR revealed that the gene expression levels of β-catenin were same in all samples. CONCLUSIONS: The accumulation of β-catenin in the cytoplasm and/or nuclei frequently occurs in hepatocarcinogenesis of rats. It may be an early event in the development of hepatocarcinoma of rats. | Qi-Ming Wang, Kai-Ming Yang, Hong-Ying Zhou, Zhen-Hai Yu, Xiao Li and Hui-Jun Yang Department of Human Anatomy, Huaxi Medical Centre of Sichuan University and Department of Radiology, West China Hospital of Sichuan University Chengdu 610041, China | 2006 | Hepatobiliary & Pancreatic Diseases International2006，5，1： | 1 |
| 8 | Evaluation of hepatitis B viral replication and proteomic analysis of HepG2.2.15 cell line after knockdown of HBx显示文摘BACKGROUND:Hepatitis B virus (HBV) is one of the major pathogens of human liver disease.Studies have shown that HBV X protein (HBx) plays an important role in promoting viral gene expression and replication.In this study we performed a global proteomic profiling to identify the downstream functional proteins of HBx,thereby detecting the mechanisms of action of HBx on virion replication.METHODS:HBx in the HepG2.2.15 cell line was knocked down by the transfection of small interfering RNA (siRNA).The replication level of HBV was evaluated by microparticle enzyme immunoassay analysis of HBsAg and HBeAg in the culture supernatant,and real-time quantitative PCR analysis of HBV DNA.Two-dimensional electrophoresis combined with MALDI-TOF/TOF was performed to analyze the changes in protein expression profile after treatment with HBx siRNA.RESULTS:Knockdown of HBx disturbed HBV replication in vitro.HBx target siRNA significantly inhibited the expression of HBsAg,HBeAg and the replication of HBV DNA.Twelve significantly changed proteins (7 upregulated and 5 downregulated) were successfully identified by MALDI-TOF/TOF using proteomics differential expression analysis after the knockdown of HBx.Among these identified proteins,HSP70 was validated by Western blotting.CONCLUSION:The results of the study indicated the positive effect of HBx on HBV replication,and a group of downstream target proteins of HBx may be responsible for this effect. | Hai-Yang Xie,Jun Cheng,Chun-Yang Xing,Jin-Jin Wang,Rong Su,Xu-Yong Wei,Lin Zhou and Shu-Sen Zheng Author Affiliations:Key Laboratory of Combined Multi-organ Transplantation,Ministry of Public Health Key Laboratory of Organ Transplantation Zhejiang Province and Division of Hepatobiliary and Pancreatic Surgery,Department of Surgery,First Affiliated Hospital,Zhejiang University School of Medicine,Hangzhou 310003,China | 2011 | Hepatobiliary & Pancreatic Diseases International2011，10，3： | 0 |
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