Basal-cell adhesion molecule (B-CAM) is induced in epithelial skin tumors and inflammatory epidermis, and is expressed at cell-cell and cell-substrate contact sites

Citation
M. Schon et al., Basal-cell adhesion molecule (B-CAM) is induced in epithelial skin tumors and inflammatory epidermis, and is expressed at cell-cell and cell-substrate contact sites, J INVES DER, 115(6), 2000, pp. 1047-1053
Citations number
33
Categorie Soggetti
Dermatology,"da verificare
Journal title
JOURNAL OF INVESTIGATIVE DERMATOLOGY
ISSN journal
0022202X → ACNP
Volume
115
Issue
6
Year of publication
2000
Pages
1047 - 1053
Database
ISI
SICI code
0022-202X(200012)115:6<1047:BAM(II>2.0.ZU;2-U
Abstract
Basal-cell adhesion molecule (B-CAM) is a 90 kDa cell surface glycoprotein of the immunoglobulin superfamily that functions as a laminin-binding recep tor. B-CAM is upregulated following malignant transformation of some cell t ypes in vivo and in vitro, thus being a candidate molecule involved in tumo r progression. As cutaneous distribution and function of B-CAM are largely unknown, we have studied its expression and regulation in normal and diseas ed human skin. In normal skin, B-CAM was expressed by endothelial cells of dermal blood vessels. In contrast, B-CAM was strongly upregulated within th e tumor tissue of both malignant and benign epithelial skin tumors, includi ng basal cell carcinomas, squamous cell carcinomas, keratoacanthomas, and c ommon warts. Transformation-associated upregulation was confirmed in vitro, but normal keratinocytes also expressed B-CAM under culture conditions. In terestingly, the basal epidermal layer of normal-appearing skin surrounding the tumors also expressed B-CAM, and B-CAM were induced on the basal and a picolateral surfaces of basal keratinocytes in inflammatory skin disorders suggesting transformation-independent mechanisms of epidermal induction of the B-CAM, Immunoelectron microscopy studies of cultured transformed kerati nocytes revealed that B-CAM was expressed at cell-cell and cell-substrate c ontact sites. Halting proliferation of transformed keratinocytes through cy tostatic drugs resulted in decreased B-CAM synthesis. Likewise, inducing te rminal differentiation in keratinocyte cultures by increasing the Ca2+ conc entration in the medium decreased B-CAM expression. In contrast, both ultra violet A and B irradiation of cultured human keratinocytes resulted in sign ificantly increased expression of the B-CAM. Overall, it appears that B-CAM expression in human skin is associated with activated states of keratinocy tes, and that B-CAM may be involved in cell-cell adhesion or migration, in addition to its known function as a laminin receptor.