Carbonic anhydrase IX reduces E-cadherin-mediated adhesion of MDCK cells via interaction with β-catenin
Eliška ŠvastováNorbert ŽilkaMiriam ZaťovičováAdriana GibadulinováFedor ČiamporJaromı́r PastorekSilvia Pastoreková
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Objective To explore the expressions of N-cadherin,E-cadherin and β-catenin in human gliomas and their significances.Methods The expressions of N-cadherin,E-cadherin and β-catenin in 42 cases of glioma tissues and 8 cases of normal brain tissues was detected by immunohistochemical S-P technique.Results The positive expressions rates of N-cadherin and β-catenin in human gliomas of grades Ⅰ-Ⅱ were significantly higher than those in normal brain tissue(P0.05),and significantly lower than those in human gliomas of grades Ⅲ-Ⅳ(P0.05).The expression of N-cadherin was positively correlated with the expression of β-catenin(r=0.778,P0.05).The positive expression rate of E-cadherin in the normal brain tissues was significantly higher than that in the gliomas(P0.05).The positive expression rate of E-cadherin in gliomas of grades Ⅰ-Ⅱ was significantly higher than that in gliomas of grades Ⅲ-Ⅳ.The expression of E-cadherin was negatively correlated with the expressions of N-cadherin and β-catenin(r1=-0.747,r2=-0.783,P0.05).Conclusions The over expressions of N-cadherin and β-catenin,and the low expression of E-cadherin may play an important role in the invasion and malignant progress of human glioma.The expressions of N-cadherin and β-catenin were closely related with the prognoses of the patient with gliomas,and may act as valuable indicators of the malignant degree of glioma and the prognosis in the patients with gliomas.
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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。
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Cadherin–catenin interactions play an important role in cadherin-mediated adhesion. Here we present strong evidence that in the cadherin–catenin complex α-catenin contributes to the binding strength of another catenin, p120, to the same complex. Specifically, we found that a β-catenin–uncoupled cadherin mutant interacts much more weakly with p120 than its full-size counterpart and that it is rapidly endocytosed from the surface of A-431 cells. We also showed that p120 overexpression stabilizes this mutant on the cell surface. Examination of the α-catenin–deficient MDA-MB-468 cells and their derivates in which α-catenin was reintroduced showed that α-catenin reinforces E-cadherin–p120 association. Finally, a cross-linking analysis of the cadherin–catenin complex indicated that a large loop located in the middle of the p120 arm-repeat domain is in close spatial vicinity to the amino-terminal VH1 domain of α-catenin. The six amino acid–long extension of this loop, caused by an alternative splicing, weakens p120 binding to cadherin. The data suggest that α-catenin–p120 contact within the cadherin–catenin complex can regulate cadherin trafficking.
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We are investigating the hypothesis that cancer progression involves the formation of abnormal cadherin-catenin complexes. The detailed analysis of cadherins and catenins expressed in a panel of 17 human bladder-cancer cell lines revealed that E-cadherin was down-regulated at the mRNA level in 5 cell lines. Interestingly, plakoglobin was also down-regulated at the mRNA level in these 5 cell lines only. Furthermore, a slower migrating form of pp120 was detected in these cell lines and in 2 cell lines with heterogeneous E-cadherin expression. Cloning of the cadherins expressed in the bladder lines revealed that P-cadherin is expressed in the lines expressing E-cadherin and down-regulated at the mRNA level in lines devoid of E-cadherin. N-cadherin was expressed in the 5 lines with reduced E-cadherin expression, in the 2 lines with heterogeneous E-cadherin expression and in 2 other cell lines. Thus, we showed that catenin changes occur in correlation with lack of E-cadherin expression and that N-cadherin becomes predominantly expressed in cells that have lost E-cadherin expression. Our data suggest that co-regulation of the expression of genes encoding different members of the classical cadherins occurs during tumor progression and that expression of some catenins is also coordinated with cadherin expression. Int. J. Cancer 82:70–76, 1999. © 1999 Wiley-Liss, Inc.
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We are investigating the hypothesis that cancer progression involves the formation of abnormal cadherin-catenin complexes. The detailed analysis of cadherins and catenins expressed in a panel of 17 human bladder-cancer cell lines revealed that E-cadherin was down-regulated at the mRNA level in 5 cell lines. Interestingly, plakoglobin was also down-regulated at the mRNA level in these 5 cell lines only. Furthermore, a slower migrating form of pp120 was detected in these cell lines and in 2 cell lines with heterogeneous E-cadherin expression. Cloning of the cadherins expressed in the bladder lines revealed that P-cadherin is expressed in the lines expressing E-cadherin and down-regulated at the mRNA level in lines devoid of E-cadherin. N-cadherin was expressed in the 5 lines with reduced E-cadherin expression, in the 2 lines with heterogeneous E-cadherin expression and in 2 other cell lines. Thus, we showed that catenin changes occur in correlation with lack of E-cadherin expression and that N-cadherin becomes predominantly expressed in cells that have lost E-cadherin expression. Our data suggest that co-regulation of the expression of genes encoding different members of the classical cadherins occurs during tumor progression and that expression of some catenins is also coordinated with cadherin expression.
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E-cadherin is a member of the cadherin family of Ca2+-dependent cell-cell adhesion molecules. p120-Catenin and δ-catenin are known to bind to similar juxtamembrane regions of E-cadherin, and p120-catenin is known to stabilize E-cadherin. However, the function of competition between p120-catenin and δ-catenin for E-cadherin has not been fully explained. In this report, we show that cells overexpressing δ-catenin contain less p120-catenin than control cells at the cell-cell interface and that this causes the relocalization of p120-catenin from the plasma membrane to the cytosol. We show that successful binding by one to E-cadherin adversely affects the stability of the other.
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The carboxyl terminus-truncated cadherin (nonfunctional cadherin) has no cell adhesion activity probably because of its failure to associate with cytoplasmic proteins called alpha and beta catenin. To rescue this nonfunctional cadherin as adhesion molecules, we constructed three cDNAs for fusion proteins between nonfunctional E-cadherin and alpha catenin, nE alpha, nE alpha N, and nE alpha C, where the intact, amino-terminal and carboxy-terminal half of alpha catenin, respectively, were directly linked to the nonfunctional E-cadherin, and introduced them into mouse L cells. The subcellular distribution and cell adhesion activity of nE alpha and nE alpha C molecules was similar to those of intact E-cadherin transfectants: they bound to cytoskeletons, were concentrated at cell-cell adhesion sites and showed strong cell adhesion activity. nE alpha N molecules, which also bound to cytoskeletons, showed very poor cell adhesion activity. Taken together, we conclude that in the formation of the cadherin-catenin complex, the mechanical association of alpha catenin, especially its carboxy-terminal half, with E-cadherin is a key step for the cadherin-mediated cell adhesion. Close comparison revealed that the behavior of nE alpha molecules during cytokinesis was quite different from that of intact E-cadherin, and that the intercellular motility, i.e., the cell movement in a confluent sheet, was significantly suppressed in nE alpha transfectants although it was facilitated in E-cadherin transfectants. Considering that nE alpha was not associated with endogenous beta catenin in transfectants, the difference in the nature of cell adhesion between nE alpha and intact E-cadherin transfectants may be explained by the function of beta catenin. The possible functions of beta catenin are discussed with a special reference to its role as a negative regulator for the cadherin-mediated cell adhesion system.
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Mouse tibial growth plates were examined for the presence of adhesion molecules using immunohistochemistry and RT-PCR. All of the components of the classical cadherin/catenin complex (cadherin, α-, β-, and γ-catenin), as well as a heavy presence of p120, were identified in the murine growth plate. All of the major cadherins (1-5, 11, 13, and 15) were, for the first time, identified and localized in the murine growth plate. We have demonstrated that most of the cadherins and catenins reside in the zone of hypertrophy. Only α-catenin and E-, P-, R-, and VE-cadherin were found in all regions of the growth plate. The results for T-cadherin were inconclusive. (J Histochem Cytochem 55: 845–852, 2007)
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检测 E-cadherin 的表情的目的，α - catenin；β - catenin；分析在 E-cadherin-catenin 粘附建筑群之间的关系；在乳癌的 clinicopathological 特征。方法 E-cadherin 的表情，α - cadherin；在 54 乳癌的标本的β - catenin，在肿瘤附近的 21 正常的胸纸巾，平常的类型的 15 胸增生；15 胸不正常的增生被免疫检测组织化学的方法。导致 21 正常的胸纸巾， E-cadherin；α - catenin 在管的房间膜上被表示；腺泡房间，出现细胞的轮廓；在房间之中的边阶。在平常的类型的胸增生的三蛋白质的染色的特性在正常的胸织物与那一样。在胸不正常的增生， E-cadherin 的反常表示率，α - catenin；β - catenin 是 6.7% ， 13.3% ；26.7% 分别地。E-cadherin-catenin 建筑群的全部的反常表示率是 33.3% 。在乳癌，反常表示 E-cadherin 评价，α - catenin；β - catenin 是 51.9% ， 63.0% ；61.1% 分别地。E-cadherin-catenin 建筑群的全部的反常表示率是 88.9% 。E-cadherin 的反常表示；α - catenin 显著地与组织学的等级被相关。α - catenin 的反常表情；β - catenin 显著地与 TNM 阶段被相关，腋的淋巴节点转移；手术后的远转移。E-cadherin-catenin 建筑群的反常表示与 TNM 阶段被相关，组织学的等级；腋的淋巴节点。β - catenin 的反常表示否定地与 HER-2 的表示被相关。艇长多重因素分析证明 E-cadherin 或α - catenin 或β - catenin 不是独立预示的指示物。E-cadherin 的结论反常表情，α - catenin；β - catenin 经常发生在乳癌。E-cadherin-catenin 建筑群的反常表示与区别骚乱被相关；转移。E-caherin 的联合测量，α - catenin；β - catenin 可以改进精确性；预言转移的敏感；乳癌的预后。
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