β-catenin和cyclin D1在乳腺癌中的表达及意义

目的探讨乳腺癌组织中β－连接素(β-catenin)、细胞周期蛋白D1(cyclin D1)的表达与乳腺癌发生、浸润及转移的关系.方法应用SP免疫组化方法检测60例乳腺癌组织中β-catenin、cyclin D1的表达.结果乳腺癌组织中有42例(70％)β-catenin异常表达,28例(46.7％)cyclin D1过度表达.β-catenin异常表达率与乳腺癌大小、分化程度及淋巴结转移与否无显著相关性,P>0.05;β-catenin在Ⅲ～Ⅳ期乳腺癌、浸润性小叶癌中的异常表达率(90%、95%)明显高于Ⅰ～Ⅱ期乳腺癌、浸润性导管癌(60%、58.3%),P<0.05,P＜0.01.cyclin D1过度表达率与乳腺癌大小、组织学类型、分化程度无显著相关性,P>0.05;与TNM分期、淋巴结转移与否有显著相关性,P<0.05.β-catenin异常表达病例中,57.1％(24/42)的病例呈现cyclin D1的过度表达,但β-catenin正常膜表达病例中,22.2％(4/18)的病例呈现cyclin D1的过度表达.β-catenin异常表达与cyclin D1过度表达有显著的正相关性,rs=0.321,P<0.05.结论β-catenin的异常表达激活cyclin D1的过度表达,引起细胞增殖和分化失控,在乳腺癌的发生中可能起着重要作用.β-catenin的异常表达不是影响乳腺癌细胞转移的主要因素,但可能是一个协同因素.     

α,β-catenin和cyclin D1在乳腺癌中的表达及意义

目的探讨乳腺癌组织中α,β-连接素（α,β-catenin）、细胞周期蛋白D1（cyclin D1）的表达与乳腺癌发生、浸润及转移的关系。方法应用S-P免疫组化方法检测60例乳腺癌组织中α,β-catenin、cyclin D1的表达。结果乳腺癌组织中有37例（61.7％）α-catenin,42例（70％）β-catenln异常表达,28例（46．7％）cyclin D1过度表达。α,β-catenin异常表达率与分化程度及淋巴结转移与否无显著相关性（P〉0．05）;α,β-catenin在浸润性小叶癌中的异常表达率（85．7％、95％）明显高于浸润性导管癌（50％、58．3％）（P〈0．05）、（P〈0．01）。cyclin D1过度表达率与乳腺癌大小、组织学类型、分化程度无显著相关性（P〉0．05）;与TNM分期、淋巴结转移与否显著相关（P〈0.05）。β-catenin异位表达病例中,57．1％（24／42）的病例出现cyclin D1的过度表达,但β-catenin正常膜表达病例中,22．2％（4／18）的病例呈现cyclin D1的过度表达。β-catenin异常表达与cyclin D1过度表达有显著的正相关性（rn=0.321,P〈0．05）。结论 β-catenin的异常表达激活cyclin D1的过度表达,引起细胞增殖和分化失控,在乳腺癌的发生中可能起着熏要作用。α,β-catenin的异常表达不是影响乳腺癌细胞转移的主要因素,但可能是一个协同因素。     

E-cadherin和β-catenin在食管鳞癌组织中的表达及其临床病理学意义

背景与目的:上皮性钙黏附蛋白(E-cadherin)不仅在介导钙离子依赖的同型细胞间的黏附中发挥作用,而且在细胞的迁徙和肿瘤浸润转移方面也有着重要的作用.许多研究表明,E-cadherin是作为一种抑癌基因发挥作用的.而最近研究表明,和E-cadherin相反,β-连环蛋白(β-catenin)在促进肿瘤的浸润转移方面具有重要作用.本研究重点探讨E-cadherin和β-catenin在食管鳞癌组织中的表达及其临床病理意义.方法:采用免疫组织化学PV法检测62例食管鳞癌组织、31例癌旁不典型增生组织及62例正常食管黏膜组织中E-cadherin和β-catenin的蛋白表达.结果:(1)正常黏膜组织、癌旁不典型增生组织及食管鳞癌组织中E-cadherin的阳性表达率依次降低,分别为95.2%、71.0%、40.3%;随着正常食管黏膜组织向癌组织的转化,β-catenin的膜表达阳性率依次降低,而胞质表达阳性率则依次增高,在低分化癌组织中甚至出现了核表达;E-cadherin的阴性表达率及β-catenin的胞质阳性表达率与食管鳞癌的浸润深度、分化程度及淋巴结转移密切相关(P＜0.05).(2)E-cadherin和β-catenin在食管鳞癌组织中的表达呈负相关(r=-0.453,P＜0.05).结论:食管鳞癌组织中E-cadherin的低表达及β-catenin的胞质高表达与食管鳞癌的浸润、转移有密切的关系.     

上皮间叶转化相关蛋白在三阴性乳腺癌组织中的联合表达及其与预后的关系

目的 检测上皮间叶转化相关蛋白E-cadherin、β-catenin和Vimentin在三阴性乳腺癌中的联合表达及其与预后的关系。方法 免疫组织化学分别检测E-cadherin、β-catenin和Vimentin在51例三阴性乳腺癌中的表达,分析其联合表达与预后的相关性。结果 E-cadherin或β-catenin表达的缺失或Vimentin表达的增高均为异常表达。3项均正常、1~2项不正常以及3项均不正常的病例数分别为1例(1.96%)、37例(72.55%)、13例(25.49%)。3项均不正常组的5年内无瘤生存较其他组明显缩短（Logrank检验,P<0.01）。结论 上皮间叶转化相关蛋白E-cadherin、β-catenin和Vimentin的联合检测有助于区分三阴性乳腺癌的异质性。     

β-catenin基因在乳腺癌中的表达和突变

 目的　探讨β-catenin基因在乳腺癌中的表达和突变情况。方法　应用免疫组织化学SP法检测119例乳腺癌、72例乳腺腺病和40例正常乳腺组织中β-catenin的表达,分析其与乳腺癌临床病理特征的关系。应用PCR和基因测序的方法检测44例乳腺癌β-catenin外显子3的突变情况。结果　40例正常乳腺组织中β-catenin在细胞膜中强表达。乳腺癌β-catenin异常表达率78.15 %（93／119）明显高于乳腺腺病44.44 %（32／72）,组间比较差异有统计学意义（P＜0.01）。β-catenin异常表达与淋巴结转移相关。44例乳腺癌组织中未检测到β-catenin基因外显子3的突变,β-catenin的异常表达率为77.30 %（34／44）。结论　β-catenin异常表达可作为评估乳腺癌转移预后、指导治疗的指标。乳腺癌组织中β-catenin异常表达不是由β-catenin基因突变所致,可能存在其他机制,有待于进一步研究。     

β-catenin通路相关基因在大肠癌组织中的表达及其临床意义

[目的]研究大肠癌组织中β-catenin、cyclinD1和c—myc蛋白的表达及临床意义。[方法]采用免疫组化法检测正常大肠黏膜和大肠癌组织中β-catenin、cyclinD1和c—mye蛋白的表达。[结果]正常大肠黏膜β-catenin蛋白表达定位于细胞膜，大肠癌组织β-catenin细胞浆和细胞核表达（异位表达）明显增加，细胞膜表达有不同程度的减少。大肠癌组织异位表达率为63．1％，细胞膜表达缺失率为70．8％，大肠癌组织β-catenin的异位表达率与肿瘤分化程度、临床分期和淋巴结转移有关。大肠癌组织中cyclinD1和c—myc表达明显高于正常大肠黏膜。大肠癌组织中β-catenin异位表达率与cyclinD1和c-myc阳性表达率均呈明显正相关。[结论]异常的β-catenin相关信号通路与大肠癌的发生发展有密切的关系，β-catenin的异常表达可能可以作为大肠癌患者诊断及预后评估的良好指标。     

β-catenin通路相关基因在大肠癌组织中的表达及其临床意义

[目的]研究大肠癌组织中β-catenin、cyclinD1和c—myc蛋白的表达及临床意义。[方法]采用免疫组化法检测正常大肠黏膜和大肠癌组织中β-catenin、cyclinD1和c—mye蛋白的表达。[结果]正常大肠黏膜β-catenin蛋白表达定位于细胞膜，大肠癌组织β-catenin细胞浆和细胞核表达（异位表达）明显增加，细胞膜表达有不同程度的减少。大肠癌组织异位表达率为63．1％，细胞膜表达缺失率为70．8％，大肠癌组织β-catenin的异位表达率与肿瘤分化程度、临床分期和淋巴结转移有关。大肠癌组织中cyclinD1和c—myc表达明显高于正常大肠黏膜。大肠癌组织中β-catenin异位表达率与cyclinD1和c-myc阳性表达率均呈明显正相关。[结论]异常的β-catenin相关信号通路与大肠癌的发生发展有密切的关系，β-catenin的异常表达可能可以作为大肠癌患者诊断及预后评估的良好指标。     

大肠癌中APC、β-catenin和cyclinD1的表达及其临床意义

目的：探讨APC、β-catenin和cyclinD1在大肠癌发生、发展过程中的作用。方法：应用免疫组织化学方法检测30例正常大肠黏膜、30例大肠腺瘤、10例大肠腺瘤恶变及50例大肠癌组织中APC、β-catenin和cyclinD1蛋白的表达情况。结果：大肠癌和大肠腺瘤恶变APC阳性率分别为44.0%,40.0%,显著低于大肠腺瘤（86.7%）和正常大肠黏膜（100%）（P〈0.01）。大肠癌、大肠腺瘤恶变和大肠腺瘤β-catenin胞浆和/或胞核异位表达率分别为：62.0%,50.0%,30.0%,显著高于正常大肠黏膜（0）（P〈0.01）,大肠癌β-catenin异位表达率显著高于大肠腺瘤（P〈0.01）。大肠癌中β-catenin膜表达缺失率为：46.0%,显著高于大肠腺瘤（10.0%）和正常大肠黏膜（0）（P〈0.01）。大肠癌、大肠腺瘤恶变、大肠腺瘤cyclinD1阳性率分别为：66.0%,60.0%,30.0%,显著高于正常大肠黏膜（0）（P〈0.01）,大肠癌cyclinD1阳性率显著高于大肠腺瘤（P〈0.01）。β-catenin膜表达缺失和cyclinD1高表达与大肠癌组织分化程度、浸润深度、淋巴结转移、Dukes分期有关。APC蛋白表达与大肠癌组织分化程度有关。大肠癌中β-catenin异位表达与cyclinD1阳性表达呈正相关关系（r=0.57,P〈0.01）,而与APC阳性表达呈负相关关系（r=-0.39,P〈0.05）。结论：APC失表达和/或β-catenin异位表达,可能是原癌基因cyclinD1激活的重要原因,并在大肠癌发生过程中起重要作用,可能是大肠癌发生的早期事件。β-catenin膜表达缺失和cyclinD1高表达与大肠癌的侵袭、转移有关。     

宫颈鳞癌及上皮内瘤变组织E-cadherin 和β-catenin及PTEN表达相关性分析

目的:探讨E-cadherin、β-catenin和PTEN在宫颈鳞癌及上皮内瘤变组织中的表达及临床意义.方法:采用免疫组化方法检测75例宫颈鳞癌、30例宫颈上皮内瘤变(CIN)及10例正常宫颈组织中E-cadherin、β-catenin和PTEN的表达.结果:正常宫颈、CINⅠ、CINⅡ～Ⅲ及宫颈鳞癌组织中E-cadherin阳性表达率依次为100.0％、85.7％、50.0％和37.3％;β-catenin异常表达率依次为0、28.6％、62.5％和84.0％;PTEN阳性表达率依次为100.0％、78.6％、56.3％和40.0％,3种蛋白在正常宫颈、CIN Ⅰ的表达与鳞癌中的表达差异均有统计学意义,在正常宫颈与CINⅡ～Ⅲ中的表达差异也均有统计学意义,P＜0.05.E-cadherin、PTEN在宫颈鳞癌中的阳性表达均与病理组织学分级、淋巴结转移及临床分期有关,P＜0.05;β-catenin异常表达与病理组织学分级、淋巴结转移有关(P＜0.05),但与临床分期无关(P＞0.05).宫颈鳞癌组织中E-cadherin与PTEN阳性表达呈正相关,与β-catenin异常表达呈负相关;β-catenin异常表达与PTEN 阳性表达呈负相关.结论:E-cadherin与PTEN表达缺失或降低及β-catenin异常表达,均在宫颈鳞癌的发生、发展及淋巴结转移中发挥重要作用,且三者之间关系密切.     

肾透明细胞癌组织E-cadherin和β-catenin及Cyclin D1表达的研究

目的:探讨E-cadherin、β-catenin及Cyclin D1在肾透明细胞癌(RCCC)中的表达及意义.方法:用免疫组化法检测E-cadherin、β-catenin及Cyclin D1在67例RCCC组织中的表达情况,并分析其与预后的关系.结果:E-cadherin及Cyclin D1在RCCC组织中表达率分别为35.8％(24/67)和44.8％(30/67).β-catenin在RCCC组织中胞膜和胞质表达率分别为23.9％(16/67)和68.7％(46/67).E-cadherin在RCCC组织中的表达与肿瘤病理分级及临床分期相关(r=0.393,P=0.001;r=0.365,P=0.002).E-cadherin与β-catenin胞膜表达之间具有显著相关性,r=0.531,P=0.000.β-catenin在RC-CC组织中胞膜表达与肿瘤临床分期相关,r=0.386,P=0.001.Cyclin D1与β-catenin胞膜表达之间具有显著相关性,r=0.481,P=0.000.Cyclin D1在RCCC中的表达与肿瘤体积大小具有相关性,r=0.325,P=0.007.结论:E-cadherin和β-catenin蛋白低表达或异常表达与RCCC的病理分级和临床分期有关,并对RCCC预后评价有一定参考意义.     

Significance of E-cadherin/beta-catenin complex and cyclin D1 in breast cancer

E-cadherin and beta-catenin are important epithelial adhesion molecules in normal epithelium. Loss of E-cadherin - beta-catenin adhesion is an important step in the progression of many epithelial malignancies. beta-catenin plays also a role in intracellular signaling and can function as an oncogene when binds to the T-cell factor 4 (Tcf4)-binding site in the promotor region of cyclin D1 and transactivates genes after translocation to the nucleus. We evaluated the immunohistochemical expression pattern of E-cadherin, beta-catenin in relationship with cyclin D1 overexpression, tumor stage, clinicopathologic parameters and patient survival in 128 mammary infiltrating duct carcinomas. The expression of E-cadherin/beta-catenin complex and beta-catenin/cyclin D1 double staining with confocal scanning laser microscope was evaluated. There were aberrant expressions in 78% of E-cadherin, 79% of beta-catenin, and 66% of cyclin D1 in breast cancer. There was correlation of aberrant expression of E-cadherin or beta-catenin with lymph node metastasis, survival rate, and survival length. However, there was no correlation of cyclin D1 overexpression with aberrant expression of E-cadherin or beta-catenin. No death was found in normal expression of beta-catenin, however lowest survival (50%) was found in nuclear beta-catenin expression. There was correlation of overexpression of cyclin D1 with survival rate and survival length. The highest survival rate and survival length were found in membranous normal beta-catenin expression group, however significant decrement of survival length was found in the groups of aberrant expression one or both of E-cadherin or/and beta-catenin. These results suggest that aberrant expression of E-cadherin, beta-catenin, and cyclin D1 may be involved in tumor metastasis, and analysis of the degree or the pattern of E-cadherin, beta-catenin, cyclin D1, and E-cadherin/beta-catenin complex may be good prognostic markers of mammary infiltrating duct carcinoma.     

The expressions and significance of α-, β-catenins and cyclin D1 in breast cancers

Objective  To study the relationship between expressions of α-, β-catenins and cyclin D1 and the occurrence, infiltration and metastasis of breast cancer. Methods  High sensitive S-P immunohistochemical method was used to detect the protein expressions of α-, β-catenins and cyclin D1 in the 60 cases of breast cancer tissues. Results  Abnormal immunoreactivities of α-and β-catenins were observed in 37 (61.7%) and 42 (70%) cases of breast cancer tissues, respectively. There were 28 cases (46.7%) who showed cyclin D1 overexpression. The abnormal expression rates of α-and β-catenins in infiltrating lobular carcinoma (ILC) were significantly higher than those in infiltrating ductal carcinoma (IDC) (P < 0.05), but they had no relations to the extent of differentiation and lymphatic metastasis of breast cancer (P > 0.05). The overexpression rate of cyclin D1 was correlated with tumor stage and lymphatic metastasis of breast cancer (P < 0.05), but not with histological type and the extent of differentiation (P > 0.05). Cyclin D1 overexpression was observed in 57.1% (24/42) of these cases that showed abnormal staining of β-catenin, but only observed in 22.2% (4/18) of these cases with normal membranous staining of β-catenin. There was a significantly positive correlation between the abnormal expression of β-catenin and overexpression of cyclin D1 (r _s = 0.321, P < 0.05). Conclusion  The abnormal expression of β-catenin may play an important role in the genesis of breast cancer by triggering cyclin D1 overexpression in breast cancer. The abnormal expressions of α-and β-catenins are not a key factor in malignant cell metastasis in breast cancer, but may also involve in the progress.     

Expression patterns of beta-catenin in in situ and invasive breast cancer.

BACKGROUND: beta-Catenin plays a central role in the E-cadherin/catenin cell-cell adhesion complex and is possibly involved in cellular signalling pathways. In this study, we evaluated the expression patterns of this molecule in in situ and invasive breast cancer. METHODS: The expression of beta-catenin was evaluated in 121 breast cancer specimens by immunohistochemistry. Its relationship to clinicopathological features was also investigated. RESULTS: Altered beta-catenin expression was found in 68% of tumours. Lobular carcinomas showed abnormal beta-catenin expression more frequently (77%) than ductal carcinomas (64%) with 46% of lobular cases showing complete absence of beta-catenin immunoreactivity. Cytoplasmic beta-catenin localization was seen only in ductal carcinomas. Aberrant beta-catenin expression was observed in 54% of ductal carcinomas in situ with highly concordant beta-catenin expression patterns in the nearby in situ and invasive components. CONCLUSIONS: Quantitative and qualitative changes in beta-catenin expression occur in a considerable proportion of in situ and invasive ductal carcinomas and are more prominent in invasive lobular carcinomas. Copyright Harcourt Publishers Limited.     

Role of COX-2, VEGF and cyclin D1 in mammary infiltrating duct carcinoma

Cyclooxygenase-2 (COX-2) has an important role in the promotion of carcinogenesis, tumor invasion and angiogenesis. Vascular endothelial growth factor (VEGF) is a proangiogenic factor that is up-regulated in various tumors. VEGF has been shown to interact with COX-derived prostaglandins in angiogenesis. Cyclin D1 gene overexpression and amplification have been shown to play a role as prognostic factors in many human cancers. To better understand the roles of these genes in mammary carcinoma, the immunohistochemical expression patterns of COX-2 and VEGF were evaluated in relationship with cyclin D1 overexpression, tumor stage, clinicopathologic parameters and patient survival in 128 mammary infiltrating duct carcinomas. The expressions of COX-2/VEGF, COX-2/cyclin D1, and VEGF/cyclin D1 were evaluated using double immunofluorescein staining with a confocal scanning laser microscope. A positive expression was seen in 41% for COX-2, 47% for VEGF, and 66% for cyclin D1 in the cases with breast cancer. There was correlation in positive expression of COX-2 or VEGF with histologic grade, lymph node metastasis, and tumor size. Conversely, a significant inverse relation was observed between VEGF and patient age. There was a correlation in overexpression of cyclin D1 with lymph node metastasis, survival rate and survival length. Significant correlations were observed between COX-2 and VEGF as well as COX-2 and cyclin D1. Co-expression of only COX-2 and VEGF was detected with significance. These results indicate that elevated COX-2 or VEGF expression or cyclin D1 overexpression is more common in breast cancer patients with poor prognostic characteristics and is partly associated with an unfavorable outcome. The present findings support the efforts to initiate clinical trials on the efficacy of COX-2 inhibitors in adjuvant treatment of breast cancer.     

β-连接素在胃癌的表达及其与患者生存的关系

背景与目的:细胞粘附功能下降是恶性肿瘤发展的关键因素。作为粘附分子的E-钙粘蛋白在维持正常组织结构方面具有非常重要的作用,但其功能的发挥,需要配体-连接素(α-、β-连接素等)的调节。为探讨β-连接素在胃癌发病机制中的作用,我们研究β-连接素在胃癌的表达情况,并分析其与临床病理特征及生存期的关系。方法:采用免疫组织化学法检测148例胃癌石蜡标本β-连接素和E-钙粘蛋白的表达水平。结果:胃癌组织β-连接素和E-钙粘蛋白的异常表达率分别为43.2%和44.6%;胃癌β-连接素和E-钙粘蛋白其中一种或二种表达异常者达63%。β-连接素和E-钙粘蛋白在低分化癌的异常表达率显著高于高分化癌(均P<0.005)。β-连接素表达异常与胃癌浸润深度密切相关(P<0.025);淋巴结转移阳性(45/84,53.6%)及发生远处转移(21/31,67.7%)的β-连接素异常表达率显著高于淋巴结转移阴性(19/64,29.7%)(P<0.005)及无远处转移者(43/117,36.8%)(P<0.005)。β-连接素正常表达比异常表达具有生存优势(P<0.005),且独立于浸润深度、淋巴结转移及分化程度。结论:胃癌广泛存在E-钙粘蛋白复合体表达异常;β-连接素异常表达是对胃癌生存期具有预测价值的重要指标。     

Prognostic significance of combined expression of MUC1 and adhesion molecules in advanced gastric cancer

The objective of the present study was to evaluate the combination of MUC1 and the status of adhesion molecules in advanced gastric cancers as a possible predictor of patient survival. Two hundred and two paraffin-embedded specimens of gastric carcinoma were examined by immunohistochemical staining using monoclonal antibodies against MUC1 mucin, E-cadherin and beta-catenin. The expression of MUC1 was considered positive if at least 10% of the neoplastic cells were stained. E-cadherin and beta-catenin were classified into four groups. Only a membranous pattern, which was stained as strongly as normal epithelial cells, was judged as normal. The absent pattern (loss of staining), cytoplasmic pattern (cytoplasmic staining with loss of membranous expression), and heterogeneous pattern (cytoplasmic staining with preservation of membranous expression) were considered abnormal. There was a significant relationship between MUC1-positive expression and abnormal expression of E-cadherin (P=0.017). The cancer with abnormal E-cadherin expression or MUC1-positive expression increased, indicating that the cancer invasion was deep. Survival analysis of the outcome revealed that the survival time for those with abnormal E-cadherin/MUC1-positive expression was shorter than for those with other expression patterns. Multivariate analysis revealed that patients with abnormal E-cadherin/MUC1-positive expression had a poorer prognosis with significance (P<0.0001). In conclusion, abnormal E-cadherin/MUC1-positive expression pattern in advanced gastric cancer is an independent unfavorable prognostic marker.     

Decreased E-cadherin augments beta-catenin nuclear localization: studies in breast cancer cell lines

We showed that the YMB-1-derived breast cancer cell line YMB-S, which proliferates in suspension without aggregation, exhibits complete loss of cell-cell adhesion despite the presence of E-cadherin-catenin complex and expression of free beta-catenin in the cytoplasm. Here, we describe beta-catenin gene regulation, interaction with E-cadherin, immunocytochemical localization, and their relation to growth rate in the YMB-1-derived cell line YMB-A, which forms tight junctions and displays anchorage-dependent growth. YMB-A cells proliferated more slowly than YMB-S cells. E-cadherin and APC gene product expression in YMB-A cells was significantly higher than that in YMB-S cells, whereas expression of beta-catenin, MUC1, and c-myc was lower in YMB-A cells than in YMB-S cells. According to immunocytochemical analysis, beta-catenin in YMB-A cells displayed membranous or submembranous localization, indicating that beta-catenin is mostly tethered to E-cadherin. Inhibition of E-cadherin expression in YMB-A cells by an antisense oligonucleotide did not change expression of whole cell beta-catenin protein, but increased nuclear beta-catenin protein level, c-myc expression, and cell growth rate. These results suggest that decreased expression of E-cadherin and APC and increased amount of beta-catenin in YMB-S cells lead to accumulation of beta-catenin in the nucleus, activate beta-catenin-LEF/TCF signaling pathway, and trigger c-myc proto-oncogene expression. c-Myc overexpression in breast cancer may be related to activated Wnt independent beta-catenin-LEF/TCF signaling.     

Adriamycin activates E-cadherin-mediated cell-cell adhesion in human breast cancer cells

E-cadherin-mediated cell-cell adhesion plays a crucial role in intercellular communication, which is related to the regulation of cell proliferation, differentiation, and apoptosis. Our previous study showed that decreased expression of MUC1 can induce E-cadherin-mediated cell-cell adhesion in human breast cancer cell lines proliferating in suspension without aggregation. Using such a cell line (YMB-S), we observed the effects of an anticancer agent, adriamycin, on cell-cell adhesion and expression of E-cadherin-catenin complex and MUC1. The cells showed E-cadherin-mediated cell-cell adhesion after 48 h exposure to 0.4 micromol/l adriamycin. And in these cells, expression of E-cadherin and beta-catenin mRNA obviously began to increase, while expression of MUC1 mRNA decreased, as demonstrated by Northern blot analysis. Such change in mRNA levels were followed by increases in E-cadherin and beta-catenin protein levels and a decrease in MUC1 protein level. Though expression of alpha-catenin mRNA began to increase on day 2, its protein level did not change. In immunohistochemical analysis, beta-catenin protein in untreated cells showed diffuse cytoplasmic localization, whereas beta-catenin in treated cells was present in cytoplasm with a clear submembranous localization, indicating that increased beta-catenin mainly bound with E-cadherin, participating in cell-cell adhesion. These findings show for the first time that adriamycin can induce E-cadherin-mediated cell-cell adhesion by increasing expression of E-cadherin and beta-catenin and decreasing expression of MUC1 during breast cancer cell apoptosis induced by this drug.