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Carcinogenesis Advance Access originally published online on August 29, 2003
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Carcinogenesis, Vol. 24, No. 12, 1879-1886, December 2003
© Oxford University Press; all rights reserved

CANCER BIOLOGY

Influence of tumor-associated E-cadherin mutations on tumorigenicity and metastasis

Marcus Kremer1,2,*, Leticia Quintanilla-Martinez2,*, Margit Fuchs1, Armando Gamboa-Dominguez3, Sieglinde Haye4, Holger Kalthoff4, Erika Rosivatz1, Christine Hermannstädter1, Raymonde Busch5, Heinz Höfler1,2 and Birgit Luber1,6

1 Technische Universität München, Klinikum rechts der Isar, Institut für Allgemeine Pathologie und Pathologische Anatomie, München, Germany, 2 GSF-Forschungszentrum für Umwelt und Gesundheit, Institut für Pathologie, Neuherberg, Germany, 3 Department of Pathology, Instituto Nacional de la Nutricion Salvador Zubiran, Mexico, D.F., Mexico, 4 Klinik für Allgemeine Chirurgie und Thoraxchirurgie, Kiel, Germany and 5 Technische Universität München, Klinikum rechts der Isar, Institut für Medizinische Statistik und Epidemiologie, München, Germany

In this study, we investigated whether tumor-associated E-cadherin mutations impair the tumor-suppressive function of the cell adhesion molecule and influence metastasis formation in a severe combined immunodeficiency mouse model. The investigated E-cadherin mutations were in frame deletions of exons 8 (del 8) or 9 (del 9) and a point mutation in exon 8 (p8). Transfected human MDA-MB-435S carcinoma cells stably expressing wild-type (wt) or mutant E-cadherin were injected into the mouse mammary fat pad. Mice transplanted with wt E-cadherin transfectants developed significantly smaller tumors than animals transplanted with the E-cadherin-negative parental cell line. Animals transplanted with del 9 or p8 E-cadherin transfectants produced medium size tumors, indicating that these mutations impair the tumor-suppressive function of E-cadherin. In contrast, mice transplanted with del 8 E-cadherin transfectants developed tumors of approximately the same sizes as animals transplanted with wt E-cadherin expressing cells. Lung metastases were induced by all cell lines without significant differences. Immunohistochemical analysis of E-cadherin expression in the tumors revealed a heterogeneous staining pattern, indicating loss or down-regulation of E-cadherin in some tumor cells. Metastases were completely negative for E-cadherin. Our data suggest that the type of mutation determines whether the tumor-suppressive function of E-cadherin is impaired.


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