E-cadherin蛋白在前列腺癌组织中的表达及临床意义

目的　探讨上皮细胞钙粘素 (E cadherin ,E Cad)在前列腺癌组织中的表达及其临床意义。方法　应用免疫组织化学 (SP)方法测定 42例前列腺癌及 3例正常和 7例良性前列腺增生组织中E Cad蛋白的表达。结果　 42例前列腺癌组织中 2 1例E Cad蛋白表达阳性 ( 5 0 %)。随肿瘤细胞病理分级、临床分期程度的增高 ,癌细胞表达E Cad蛋白阳性率降低 ,高、中分化组 2 2例前列腺癌中 19例E Cad蛋白表达阳性( 86%) ,与低分化组 2 0例中 2例 ( 10 %)阳性表达 ;A +B期和C +D期前列腺癌组织中的阳性表达率分别为 65 5 %( 19/ 2 9)和 15 3 %( 2 / 13 ) ,各组间比较有显著性差异 ( χ2 =2 4 43 ,P <0 0 0 5 ;χ2 =9 0 3 ,P <0 0 0 5 )。而正常和良性前列腺增生组E Cad蛋白均呈阳性免疫反应。结论　E Cad蛋白异常表达在前列腺癌的恶性进展中起重要作用 ,检测E Cad蛋白的表达有利于判断病期及预后。     

钙粘素和增殖相关抗原在非小细胞肺癌中的表达及临床意义

目的 探讨上皮钙粘素(E-cd)和增殖相关抗原(Ki67)在非小细胞肺癌(NSCLC)中的表达及癌细胞发生侵袭、转移过程中的意义。方法 收集62例NSCSLC患者标本，采用免疫组化S-P法检测E-cd和Ki67抗原的表达水平。结果 E-cd在Ⅲ～Ⅳ期和Ⅰ～Ⅱ期的阳性表达率分别为33．3％和65．7％，Ki67在Ⅲ～Ⅳ期和Ⅰ～Ⅱ期的阳性表达率分别为(96．3％)和(68．6％)，伴有或不伴有癌旁转移的NSCLC病例间其E-cd和Ki67阳性表达水平差异均有显著性意义。结论 E-cd和Ki67的表达水平与NSCLC侵袭、转移密切相关，且二者在NSCLM中的表达呈显著负相关。     

Cell adhesion molecules in the formation of liver metastasis

Metastasis is the most life-threatening event in patients with cancer, with the liver being one of the most frequently affected organs. In the development and establishment of metastasis, blood-borne cancer cells utilise various cell adhesion mechanisms (cell-cell, cell matrix, tumour-endothelial and hepatocyte). Thus, cell adhesion molecules have a pivotal role in this process of metastasis formation. This article discusses recent progress in the biology of cell adhesion molecules in the formation of liver metastasis and the clinical implications of the findings. Received for publication on Jan. 6, 1998; accepted on June 20, 1998     

出生前后大鼠心肌细胞钙粘蛋白的表达

目的　探讨出生前后大鼠心肌细胞钙粘蛋白 (cadherin)的表达和分布变化规律。方法　应用S P免疫组化方法分别检测孕 16d胎鼠、出生后 2d、5d和 10d的新鲜大鼠心脏标本 ,观察心肌细胞cadherin的表达和分布。结果　心肌细胞cadherin在大鼠的心房、心室、乳头肌、室间隔等处均有表达。胎鼠和出生后 2d大鼠心肌细胞中cadherin分散地分布于细胞表面和胞浆中 ;出生后 5～ 10d大鼠心肌细胞cadherin大部分分布在心肌细胞的闰盘处 ,少部分分布在细胞膜上和胞浆中。结论　在大鼠心肌发育过程中 ,以cadherin介导的细胞间机械偶联经历了动态变化 ,与闰盘的发育相一致     

肿瘤浸润抑制因子在喉癌复发及转移中的作用

目的 :研究肿瘤浸润抑制因子 (E cadherin)在喉癌复发、转移中的作用 ,以探讨喉癌复发转移的机制。方法 :利用PCR、PCR SSCP等分子生物学方法 ,检测E cadherin基因第 5、7对外显子在喉癌组织中的基因突变。结果 :正常喉组织有E cadherin基因表达 ,无基因突变 ;癌旁组织第 5对外显子突变率为 2 .5 %。第 5、7对外显子在喉复发癌组织中的基因突变率分别为 2 8.5 7%、0 % ;淋巴结转移阳性组分别为 4 7.0 6%、64.71% ,淋巴结转移阴性组分别为 0 %、6.2 5 % ;且基因突变率随肿瘤TNM临床分期而增高。结论 :通过对喉癌组织中E cadherin基因突变的检测 ,可以判断肿瘤复发、转移的倾向性 ;E cadherin基因突变可能是喉癌复发、转移的分子机制之一     

Expression of cadherins and catenins in oral epithelial dysplasia and squamous cell carcinoma

The immunocytochemical expression of cadherins and catenins was examined during the process of oral carcinogenesis by comparing their expression in normal and dysplastic epithelium with primary and metastatic carcinomas. While control epithelium showed normal distribution for P and E cadherin and the catenins, in severe dysplasia P-cadherin was upregulated. In other cases and in carcinoma- in-situ adjacent to infiltrating carcinomas, membranous expression of the cadherins and catenins was reduced or lost. The changes in expression of E-cadherin and the catenins suggest that disruption of the E-cadherin/catenin complex is a late event associated with invasion. In primary carcinomas reduced membranous and cytoplasmic staining were observed for both cadherins and catenins. Abnormal localisation of E-cadherin occurred in the more superficial parts of the better differentiated carcinomas, suggesting abnormality to the E-cadherin complex(es). In contrast, membranous expression of cadherins and catenins was reduced or lost in the deep invasive margin of primary carcinomas and in most poorly differentiated carcinomas. For E-cadherin at least, this reduction appears associated with differentiation, invasion and possibly prognosis. Possible mechanisms involved for changes in expression of the cadherins and associated catenins and areas for further study are discussed.     

非小细胞肺癌E-钙粘蛋白基因异常的研究

目的 观察非小细胞肺癌组织中E—钙粘蛋白(E—cadherin）的基因异常。方法 采用PCR—SSCP及序列分析，研究了24例非小细胞患者肺癌组织中E—cadherin基因外显子6、7、8、9的基因突变。结果 24例非小细胞肺癌中发现2例存在E—cadhetrin exon9的基因插入、缺失及突变。结论 E—cadherin在非小细胞肺癌中存在基因异常改变，尤其集中在E—cadherin的细胞外区域，主要表现为插入及缺失，细胞外区域的某因异常改变可能是赞成上皮细胞粘附力下降的主要原因。     

Modulation of cellular adhesion in bovine brain microvessel endothelial cells by a decapeptide

The importance of cell adhesion molecules in maintaining the cellular integrity of the endothelial layer is well recognized, yet their exact participation in regulating the blood–brain barrier (BBB) is poorly understood. Both Ca²⁺-dependent and Ca²⁺-independent cell adhesion molecules are found in endothelial cells. In this study, we used immunofluorescence, ELISA, Western blot and cell adhesion assay to identify a Ca²⁺-dependent cell adhesion molecule, E-cadherin, in bovine brain microvessel endothelial cells (BBMECs). Monoclonal anti-E-cadherin antibody specifically interacted with cultured BBMECs and decorated the cellular junctions with a series of punctate fluorescence spots as seen by indirect immunofluorescence using a confocal microscope. The intensity of these fluorescence spots increased after brief treatment with hIFN-γ or CPT-cAMP. In the cellular extract of BBMECs, a 120 kDa protein was immunoprecipitated with anti-E-cadherin antibody. BBMECs did not react with anti-N-cadherin antibody, but recognized the FITC-labeled LRAHAVDVNG-NH₂, a decapeptide generated from the EC-1 domain of N-cadherin, which decorated the lateral margins of the cells with fluorescence spots. A concentration-dependent binding of this decapeptide was also observed in the flow cytometry assay. BBMECs dissociated with trypsin plus Ca²⁺ were able to reaggregate only in the presence of Ca²⁺. However, such cell-cell aggregations of BBMECs were prevented by the presence of either anti-E-cadherin antibody or the decapeptide in the assay medium. These results confirm that BBMECs possess a distinct Ca²⁺-dependent cell adhesion mechanism that can be modulated by the decapeptide. This modulation of cell-cell adhesion in BBMECs by the decapeptide is thought-provoking for creating channels for paracellular drug delivery across the BBB.