Epithelial glycoprotein-2 expression is subject to regulatory processes in epithelial-mesenchymal transitions during metastases

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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. / Jojović, M; Adam, E; Zangemeister-Wittke, U; Schumacher, U.

In: Histochem J, Vol. 30, No. 10, 10.1998, p. 723-9.

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@article{f31016a35e3447528fee1c7a61d80451,
title = "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",
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.",
keywords = "Animals, Antibodies, Monoclonal, Antigens, Neoplasm, Breast Neoplasms, Caco-2 Cells, Cell Adhesion Molecules, Colonic Neoplasms, Female, Gene Expression Regulation, Neoplastic, HT29 Cells, Humans, Immunoenzyme Techniques, Lung Neoplasms, Mice, Mice, Inbred BALB C, Mice, SCID, Neoplasm Metastasis, Neoplasm Transplantation, Ovarian Neoplasms, Tumor Cells, Cultured",
author = "M Jojovi{\'c} and E Adam and U Zangemeister-Wittke and U Schumacher",
year = "1998",
month = oct,
language = "English",
volume = "30",
pages = "723--9",
number = "10",

}

RIS

TY - JOUR

T1 - Epithelial glycoprotein-2 expression is subject to regulatory processes in epithelial-mesenchymal transitions during metastases

T2 - an investigation of human cancers transplanted into severe combined immunodeficient mice

AU - Jojović, M

AU - Adam, E

AU - Zangemeister-Wittke, U

AU - Schumacher, U

PY - 1998/10

Y1 - 1998/10

N2 - 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.

AB - 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.

KW - Animals

KW - Antibodies, Monoclonal

KW - Antigens, Neoplasm

KW - Breast Neoplasms

KW - Caco-2 Cells

KW - Cell Adhesion Molecules

KW - Colonic Neoplasms

KW - Female

KW - Gene Expression Regulation, Neoplastic

KW - HT29 Cells

KW - Humans

KW - Immunoenzyme Techniques

KW - Lung Neoplasms

KW - Mice

KW - Mice, Inbred BALB C

KW - Mice, SCID

KW - Neoplasm Metastasis

KW - Neoplasm Transplantation

KW - Ovarian Neoplasms

KW - Tumor Cells, Cultured

M3 - SCORING: Journal article

C2 - 9873999

VL - 30

SP - 723

EP - 729

IS - 10

ER -