Nuclear translocation of β‐catenin synchronized with loss of E‐cadherin in oral epithelial dysplasia with a characteristic two‐phase appearance

Abstract

Alvarado C G, Maruyama S, Cheng J, Ida‐Yonemochi H, Kobayashi T, Yamazaki M, Takagi R & Saku T (2011) Histopathology59, 283–291 Nuclear translocation of β‐catenin synchronized with loss of E‐cadherin in oral epithelial dysplasia with a characteristic two‐phase appearance Aims: One of the important histopathological characteristics of oral epithelial dysplasia is a two‐phase appearance of rete processes, comprising an upper layer of keratinized cells and a lower layer of basaloid cells, and thereby creating a sharp contrast between these two separate cell populations. The aim of this study was to determine the cellular adhesion status of the basaloid cells. Methods and results: Immunohistochemistry for β‐catenin, E‐cadherin and their related molecules was carried out in surgical specimens of two‐phase epithelial dysplasia of the oral mucosa. The lower‐half basaloid cells and the upper keratinized cells were microdissected separately, and extracted DNA samples were subjected to methylation‐specific polymerase chain reaction amplification for E‐cadherin. β‐Catenin was immunolocalized within the nuclei and cytoplasm of Ki67‐positive lower‐half basaloid cells, as well as on the cell membrane of upper parakeratotic cells. The basaloid cells of the lower‐half were also positive for matrix metalloproteinase‐7 and cyclin D1, β‐catenin target gene products, α‐dystroglycan, tenascin‐C, and perlecan, but not for E‐cadherin. The promoter region of the E‐cadherin gene was hypermethylated. Conclusions: The solid proliferation of lower‐half E‐cadherin‐free basaloid cells is enhanced by Wnt signalling cascades, as well as by the intraepithelial extracellular matrix or its bound growth factors.