EPIDERMAL-CELL ADHESION AND BASEMENT-MEMBRANE ALTERATIONS IN EXPERIMENTAL SKIN TUMOR-DEVELOPMENT

Citation
M. Makinen et al., EPIDERMAL-CELL ADHESION AND BASEMENT-MEMBRANE ALTERATIONS IN EXPERIMENTAL SKIN TUMOR-DEVELOPMENT, Anticancer research, 18(2A), 1998, pp. 877-884
Citations number
32
Categorie Soggetti
Oncology
Journal title
ISSN journal
02507005
Volume
18
Issue
2A
Year of publication
1998
Pages
877 - 884
Database
ISI
SICI code
0250-7005(1998)18:2A<877:EAABAI>2.0.ZU;2-A
Abstract
Background: Epidermal cell adhesion and basement membrane (BM) are ess ential for the differentiated structure of squamous epithelium, and bo th are reduced in malignant tumours. Materials and Methods: We analyse d the expression of cell adhesion-related proteins desmoplakin and E-c adherin, BM components laminin and collagen IV, and BM receptor integr in a6 in experimental preneoplastic changes and neoplasms of skin. Dif ferent mouse strains (NMRI, C57Bl/6 and DBA/2) and exposure protocols (DMBA, UV, DMBA + UV) were used to find possible differences in the ex pression of cell adhesion and BM proteins within individual tumonr typ es. Results: The individual strain had an impressive role on the expre ssion of tumors. The exposure model affected the type of tumour found and tumour behaviour: The location and expression of cell attachment p roteins were dependent on morphology, brit mouse str ain and type of e xposure had no effect. The decline in the expression of markers studie d was gradual involving the cytoplasmic immunoreactivity of integrin a 6 and laminin observed in dysplastic epidermis, BM structure formation becoming increasingly disturbed in dysplasia; this was present in squ amous cell carcinomas and absent in undifferentiated tumours. Desmopla kin expression gradually disappeared during the decline in differentia tion. E-cadherin expression was preserved longer, and disappeared alon g with the loss of squamous properties. Conclusions: Desmoplakin and E -cadherin served in this study as differentiation markers. None of the se proteins seem to explain the differences in the tumonr sensitivity of individual mouse strains.