From normal respiratory mucosa to epidermoid carcinoma: Expression of human mucin genes

Citation
Mc. Copin et al., From normal respiratory mucosa to epidermoid carcinoma: Expression of human mucin genes, INT J CANC, 86(2), 2000, pp. 162-168
Citations number
21
Categorie Soggetti
Onconogenesis & Cancer Research
Journal title
INTERNATIONAL JOURNAL OF CANCER
ISSN journal
00207136 → ACNP
Volume
86
Issue
2
Year of publication
2000
Pages
162 - 168
Database
ISI
SICI code
0020-7136(20000415)86:2<162:FNRMTE>2.0.ZU;2-S
Abstract
Mucous cells in the respiratory tract contribute to the maintenance of the normal epithelial cell population via mechanisms of cell proliferation and differentiation. Mucous cell hyperplasia often occurs as a basic response t o injury in the tracheobronchial epithelium. These cells are also thought t o be involved in the histogenesis of epidermoid metaplasia, A typical bioch emical feature of these cells is mucus secretion. Aberrant glycosylation or under-glycosylation of mucins is well known in cancer; however, the specif ic role played by mucin genes is at present unclear, To provide information regarding the expression of these genes in squamous metaplasia and squamou s cell carcinoma, we analyzed and compared the expression of MUC1-MUC7 gene s by in situ hybridization in control respiratory mucosa and lesions associ ated with neoplasia (hyperplasia, metaplasia and dysplasia) and squamous ce ll carcinomas. MUC4 was expressed independently of mucus secretion since it was expressed weakly by basal cells and probably by ciliated cells as well as collecting ducts, epidermoid metaplasia with complete squamous cell dif ferentiation, and most of epidermoid carcinomas even well differentiated an d keratinized. In squamous metaplasia and dysplasia, MUC4 gene expression w as diffuse and less intense than in normal epithelium. MUC5AC was overexpre ssed in dysplasia as well as in mucous cell and basal cell hyperplasia and undetectable when squamous differentiation was achieved. Int J. Cancer 86:1 62-168, 2000. (C) 2000 Wiley-Liss, Inc.