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Cytoplasmic expression of E‐cadherin and β‐Catenin correlated with LOH and hypermethylation of the APC gene in oral squamous cell carcinomas
Author(s) -
Gao Shan,
Eiberg Hans,
Krogdahl Annelise,
Liu ChungJi,
Sørensen Jens Ahm
Publication year - 2005
Publication title -
journal of oral pathology and medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.887
H-Index - 83
eISSN - 1600-0714
pISSN - 0904-2512
DOI - 10.1111/j.1600-0714.2004.00275.x
Subject(s) - cadherin , catenin , gene , cancer research , cytoplasm , biology , cell , basal cell , pathology , genetics , medicine , wnt signaling pathway
Background: Inactivation of the adenomatous polyposis coli ( APC ) gene results in accumulation and translocation of β‐Catenin, which are important for malignant development. The aim of the present study is to investigate the possible role of APC/ β ‐Catenin pathway in oral squamous cell carcinomas. Methods: The DNA from 34 patients was examined for loss of heterozygosity (LOH) at two markers surrounding the APC , and for hypermethylation of the APC promoter by using methylation‐specific polymerase chain reaction (MS‐PCR). Fifteen of 34 samples were stained immunohistochemically to show the expression of E‐cadherin and β ‐Catenin. Results: We found that cytoplasmic rather than membrane staining of E‐cadherin and β ‐Catenin was a prominent aberrant tumour‐related alteration, and that this expression was mainly present in moderately and poorly differentiated tumours. LOH and hypermethylation of the APC promoter was found in four of 31 and five of 34 carcinoma samples, respectively. Four of five cases presenting LOH/hypermethylation showed cytoplasmic expression of E‐cadherin and β ‐Catenin by immunohistochemical (IHC) staining. Conclusion: The present results indicate that LOH at the APC locus or hypermethylation of the APC promoter 1a may lead to free β ‐Catenin accumulation in cytoplasm of oral carcinoma cells and thereby to oral malignant progression.