Epithelial cell adhesion molecule is overexpressed in hypopharyngeal carcinoma and suppresses the metastasis and proliferation of the disease when downregulated.

The epithelial cell adhesion molecule (EpCAM) is overexpressed in the majority of human epithelial carcinomas, and its overexpression is associated with proliferation and neoplastic transformation. However, the precise molecular mechanism involved in EpCAM-related proliferation and metastasis in hypopharyngeal carcinoma is unknown. The aim of the present study was to identify the role of EpCAM in the metastasis and proliferation of hypopharyngeal carcinoma. An immunohistochemical staining assay indicated that EpCAM was overexpressed in primary hypopharyngeal carcinoma tissues, and that this overexpression correlated with the tumor size and lymph node metastasis. In the following treatment of the hypopharyngeal carcinoma Fa Du cell line with EpCAM, the downregulation of EpCAM was found to significantly suppress cell metastasis and proliferation, as detected by Transwell, clone formation and MTT assays. Additionally, western blot analysis revealed that EpCAM downregulation increased the expression of the adhesion- and proliferation-related factors, E-cadherin, alpha-catenin and beta-catenin, in the cytoskeleton, as well as beta-catenin expression in the nucleus. In conclusion, the present study indicated that EpCAM is a potential oncogene and contributes to the metastasis of hypopharyngeal carcinoma. The current study is the first to provide evidence for the potential value of targeting EpCAM in hypopharyngeal carcinoma therapy.