Differential expression of laminin-5 subunits and integrin receptors in human colorectal neoplasia

Détails

ID Serval
serval:BIB_E10030DD7993
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Differential expression of laminin-5 subunits and integrin receptors in human colorectal neoplasia
Périodique
Journal of Pathology
Auteur⸱e⸱s
Sordat  I., Bosman  F. T., Dorta  G., Rousselle  P., Aberdam  D., Blum  A. L., Sordat  B.
ISSN
0022-3417 (Print)
Statut éditorial
Publié
Date de publication
05/1998
Volume
185
Numéro
1
Pages
44-52
Notes
Journal Article
Research Support, Non-U.S. Gov't --- Old month value: May
Résumé
Cell-matrix interactions contribute to regulating the adhesion, growth, migration, and differentiation of epithelial intestinal cells. Alterations in matrix components and their cellular receptors have been found in tumours but their specific roles remain unclear. The tissue patterns of laminin-5 and alpha 3, beta 3 and gamma 2 subunits, as well as those of the alpha 3, alpha 6, beta 1, and beta 4 integrin chains, were determined by immunofluorescence on frozen sections of 12 colorectal mucosal samples from four patients, 15 adenomas, 29 adenocarcinomas, and eight metastases. Distinct patterns of laminin-5 and integrin expression were found along the mucosa-adenoma, and adenoma-carcinoma transitions. Expression of basement membrane laminin-5 and subunits was continuous and gradient-like in normal mucosa, enhanced at the periphery of adenomas, and discontinuous in places in carcinomas and metastases. Decrease of the alpha 3 integrin chain was found in adenomas, together with that of alpha 6 and beta 4 chains in carcinomas. A subpopulation of carcinoma cells dissociating (budding) from neoplastic tubules was found to accumulate the laminin-5 beta 3 gamma 2 heterodimer in the cytoplasm, with progressive loss of surface integrin expression. These results suggest that in colorectal cancer, an abnormal expression of laminin-5 subunits and integrin chains may identify a subset of carcinoma cells prone to invade focally and to contribute to disease aggressiveness.
Mots-clé
Adenocarcinoma/metabolism Adenoma/metabolism Cell Adhesion Molecules/*metabolism Colon/metabolism Colorectal Neoplasms/*metabolism/pathology Fluorescent Antibody Technique, Indirect Humans Integrins/*metabolism Intestinal Mucosa/metabolism Liver Neoplasms/metabolism/secondary Microscopy, Confocal Neoplasm Proteins/*metabolism
Pubmed
Web of science
Création de la notice
25/01/2008 16:48
Dernière modification de la notice
20/08/2019 17:05
Données d'usage