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Journal of Histochemistry and Cytochemistry, Vol. 51, 921-929, July 2003, Copyright © 2003, The Histochemical Society, Inc.

ARTICLE

Alterations of Collagen XVII Expression During Transformation of Oral Epithelium to Dysplasia and Carcinoma

Mataleena Parikkaa, Tiina Kainulainenb, Kaisa Tasanenc, Anu Väänänena, Leena Bruckner–Tudermand, and Tuula Saloa
a Department of Diagnostic and Oral Medicine, University of Oulu, and Oulu University Hospital, Oulu, Finland
b Department of Prosthetic Dentistry and Stomatognathic Physiology, University of Oulu, Oulu, Finland
c Department of Dermatology, Oulu University Hospital, Oulu, Finland
d Department of Dermatology, University Hospital Münster, Münster, Germany

Correspondence to: Tuula Salo, Inst. of Dentistry, University of Oulu, Box 5281, 90014 Oulu, Finland. E-mail: Tuula.Salo@oulu.fi

Collagen XVII (BP180) is a hemidesmosomal transmembrane component that has been hypothesized to participate in keratinocyte adhesion and motility. Using immunohistochemical (IHC) and in situ hybridization (ISH) methods, we showed downregulation of collagen XVII in basal cells in mild dysplasias and upregulation in suprabasal keratinocytes in moderate and severe dysplasias as well as in the central cells of grade II and III squamous cell carcinomas (SCCs). Overexpression of collagen XVII was found at the invasive front of the tumors. Collagen XVII and its cleaved ectodomain were characterized from culture extracts and precipitates of oral keratinocytes, tongue carcinoma cells, and tumor tissue extract. Malignant cell lines exhibited increased collagen XVII expression in immunoblotting analysis. In oral keratinocytes, collagen XVII gene expression was significantly induced by PMA but not by the inflammatory cytokines TGF-ß1, TNF-{alpha}, EGF, IL-1ß, and IL-6. These results indicate altered expression of collagen XVII at different stages of carcinogenesis and suggest a correlation between overexpression of collagen XVII and tumor progression. The reduced collagen XVII expression at the early step of carcinogenesis may reflect disturbed keratinocyte adhesion to the basement membrane.

(J Histochem Cytochem 51:921–929, 2003)

Key Words: BPAG2, adhesion molecules, cancer, mouth neoplasms


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