The Histochemical Journal

, Volume 30, Issue 10, pp 723–729

Epithelial Glycoprotein-2 Expression is Subject to Regulatory Processes in Epithelial–mesenchymal Transitions During Metastases: an Investigation of Human Cancers Transplanted into Severe Combined Immunodeficient Mice


  • Milan Jojović
    • Anatomical Institute, University Hospital EppendorfUniversity of Hamburg
  • Elizabeth Adam
    • Human MorphologyUniversity of Southampton
  • Uwe Zangemeister-Wittke
    • Division of Oncology, Department of Internal MedicineUniversity Hospital ZOrich
  • Udo Schumacher
    • Anatomical Institute, University Hospital EppendorfUniversity of Hamburg

DOI: 10.1023/A:1003486630314

Cite this article as:
Jojović, M., Adam, E., Zangemeister-Wittke, U. et al. Histochem J (1998) 30: 723. doi:10.1023/A:1003486630314


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 (SoTü 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) re acted 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.

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© Kluwer Academic Publishers 1998