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Abstract

The human cell-surface antigen epithelial glycoprotein-2 recognized by the monoclonal antibody MOC-31 is an epithelial tumour-associated glycoprotein expressed in non-squamous carcinomas. MOC-31 immunoreactivity was investigated in human breast, colon, ovarian and lung cancer cell lines, grown either in vitro or in severe combined immunodeficient (SCID) mice as solid tumours and/or metastases. Three of four small-cell lung cancer cell lines (NCI-H69, OH3 and SW2) and three of four ovarian cancer cell lines (SoTu 1, 3 and 4) expressed epithelial glycoprotein-2. In contrast, all three breast (MCF-7, BT20, T47D) and all three colon (HT29, CACO2, SW480) cancer cell lines strongly reacted with monoclonal antibody MOC-31. A notable difference in MOC-31 immunoreactivity was observed in spontaneously formed lung metastases of HT29 colon cancer cells. Whereas larger metastases (> 30 cells) reacted with a similar staining pattern to the primary tumour, smaller metastases did not. These findings indicate that differentiation processes during the epithelial-mesenchymal transition occur in metastases, which lead to a transient loss of epithelial glycoprotein-2 expression during the migratory and early post-migratory period. This loss of antigen expression indicates that the process of metastases formation is a regulatory event, and this transient loss of antigen expression might represent a potential obstacle to antibody-based therapy in the setting of minimal residual disease.

EpCAM is overexpressed in local and metastatic prostate cancer, suppressed by chemotherapy and modulated by MET-associated miRNA-200c/205

“…Accordingly, Jojovic et al , described a dynamic expression of EpCAM in human cancer cells after xenotransplantation in immunocompromised mice. In this study, EpCAM was strongly expressed in primary tumours and metastases comprised of >30 cells, while it was substantially reduced in small metastases (<30 cells; Jojovic et al , 1998). In line with these findings, EpCAM is frequently reduced or missing in CTCs and DTCs (Gorges et al , 2012; Driemel et al , 2013).…”

Negative enrichment by immunomagnetic nanobeads for unbiased characterization of circulating tumor cells from peripheral blood of cancer patients

“…Consequently, CTCs that do not express EpCAM at sufficient levels could be missed by these assays, which may limit the sensitivity, and could potentially lead to a loss of particular cell subpopulations. Indeed, heterogeneous expression of epithelial surface markers has been previously reported in different tumor entities at tissue level [23,24], as well as the loss of EpCAM expression in the case of epithelial-mesenchymal transformation [25,26]. …”

EpCAM and its potential role in tumor-initiating cells

“…45 Already at this time, it was postulated that EpCAM was subject to "regulatory processes in epithelial-mesenchymal transitions during metastases." This is in line with a function of EpCAM as a cell adhesion molecule and as a promoter of cell proliferation.…”