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Expression and function of epithelial cell adhesion molecule EpCAM: Where are we after 40 years?
Cancer Metastasis Rev. 39, 969–987 (2020)
EpCAM (epithelial cell adhesion molecule) was discovered four decades ago as a tumor antigen on colorectal carcinomas. Owing to its frequent and high expression on carcinomas and their metastases, EpCAM serves as a prognostic marker, a therapeutic target, and an anchor molecule on circulating and disseminated tumor cells (CTCs/DTCs), which are considered the major source for metastatic cancer cells. Today, EpCAM is reckoned as a multi-functional transmembrane protein involved in the regulation of cell adhesion, proliferation, migration, stemness, and epithelial-to-mesenchymal transition (EMT) of carcinoma cells. To fulfill these functions, EpCAM is instrumental in intra- and intercellular signaling as a full-length molecule and following regulated intramembrane proteolysis, generating functionally active extra- and intracellular fragments. Intact EpCAM and its proteolytic fragments interact with claudins, CD44, E-cadherin, epidermal growth factor receptor (EGFR), and intracellular signaling components of the WNT and Ras/Raf pathways, respectively. This plethora of functions contributes to shaping intratumor heterogeneity and partial EMT, which are major determinants of the clinical outcome of carcinoma patients. EpCAM represents a marker for the epithelial status of primary and systemic tumor cells and emerges as a measure for the metastatic capacity of CTCs. Consequentially, EpCAM has reclaimed potential as a prognostic marker and target on primary and systemic tumor cells.
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Publication type
Article: Journal article
Document type
Review
Keywords
Epcam ; Carcinoma ; Metastasis ; Regulated Intramembrane Proteolysis ; Liquid Biopsy ; Epithelial-to-mesenchymal Transition; Circulating Tumor-cells; Breast-cancer Patients; Monoclonal-antibody Therapy; Amyloid Precursor Protein; To-mesenchymal Transition; Ep-cam; Colorectal-carcinoma; Colon-cancer; Phase-i; Intratumoral Heterogeneity
ISSN (print) / ISBN
0167-7659
e-ISSN
1573-7233
Journal
Cancer and Metastasis Reviews
Quellenangaben
Volume: 39,
Pages: 969–987
Publisher
Springer
Publishing Place
Dordrecht, Netherlands
Non-patent literature
Publications
Reviewing status
Peer reviewed
Institute(s)
CCG Personalized Radiotherapy in Head and Neck Cancer (KKG-KRT)