Cell adhesion molecule uvomorulin expression in human breast cancer cell lines: relationship to morphology and invasive capacities.
Cell adhesion molecule uvomorulin expression in human breast cancer cell lines: relationship to morphology and invasive capacities.
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人乳腺癌细胞系中细胞粘附分子 uvomorulin 的表达：与形态和侵袭能力的关系。
DOI：
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发表时间：
1991
期刊：
影响因子：
--
通讯作者：
S. Byers
中科院分区：
文献类型：
--
作者：
C. Sommers;Erik W. Thompson;J. Torri;R. Kemler;E. Gelmann;S. Byers
癌细胞中细胞间粘附的丧失可能是获得侵袭性转移表型的重要步骤。我们检测了上皮特异性细胞粘附分子uvomorulin （E-cadherin, cell- cam 120/80, L-CAM）在人乳腺癌细胞系中的表达。我们发现，纤维母细胞样，高度侵袭性，表达静脉蛋白的乳腺癌细胞系不表达乌莫霉素。在更上皮化、侵袭性更小、表达角蛋白的乳腺癌细胞系中，有些表达乌莫霉素，有些则不表达。我们检查了重组基底膜基质Matrigel中细胞系的形态，并测量了细胞穿过基质膜覆盖过滤器的能力，作为癌细胞从邻近细胞脱离并通过基底膜侵入周围组织的体外模型。在Matrigel中，uvomorulin阳性细胞的菌落具有典型的融合外观，而uvomorulin阴性细胞则表现为分离。乌莫霉素阴性和波形蛋白阳性的细胞在基质中呈星状形态。我们发现uvomorulin对Matrigel中的融合集落形态负责，因为uvomorulin阳性MCF-7细胞与uvomorulin抗体处理导致细胞彼此分离，但不会诱导这些细胞的侵袭性，这是通过在改进的Boyden室试验中通过Matrigel涂层聚碳酸酯过滤器的能力来测量的。两种uvomorulin阴性和vimentin阴性的细胞系也不具有高度侵袭性。我们认为uvomorulin介导的细胞-细胞粘附的丧失可能是参与癌细胞向侵袭性表型发展的许多变化之一。
Loss of cell-cell adhesion in carcinoma cells may be an important step in the acquisition of an invasive, metastatic phenotype. We have examined the expression of the epithelial-specific cell adhesion molecule uvomorulin (E-cadherin, cell-CAM 120/80, L-CAM) in human breast cancer cell lines. We find that fibroblastoid, highly invasive, vimentin-expressing breast cancer cell lines do not express uvomorulin. Of the more epithelial-appearing, less invasive, keratin-expressing breast cancer cell lines, some express uvomorulin, and some do not. We examined the morphologies of the cell lines in the reconstituted basement membrane matrix Matrigel and measured the ability of the cells to traverse a Matrigel-coated filter as in vitro models for detachment of carcinoma cells from neighboring cells and invasion through basement membrane into surrounding tissue. Colonies of uvomorulin-positive cells have a characteristic fused appearance in Matrigel, whereas uvomorulin-negative cells appear detached. Cells which are uvomorulin negative and vimentin positive have a stellate morphology in Matrigel. We show that uvomorulin is responsible for the fused colony morphology in Matrigel since treatment of uvomorulin-positive MCF-7 cells with an antibody to uvomorulin caused the cells to detach from one another but did not induce invasiveness in these cells, as measured by their ability to cross a Matrigel-coated polycarbonate filter in a modified Boyden chamber assay. Two uvomorulin-negative, vimentin-negative cell lines are also not highly invasive as measured by this assay. We suggest that loss of uvomorulin-mediated cell-cell adhesion may be one of many changes involved in the progression of a carcinoma cell to an invasive phenotype.
细胞间粘附糖蛋白细胞-CAM 120/80在正常人体组织和肿瘤中的表达。
DOI：
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发表时间：
1989
期刊：
The American journal of pathology
影响因子：
--
作者：
Eidelman,S;Damsky,CH;Wheelock,MJ;Damjanov,I
通讯作者：
Damjanov,I
影响因子：
56.9
作者：
FEARON, ER;CHO, KR;VOGELSTEIN, B
通讯作者：
VOGELSTEIN, B