Characterization of Wnt-1 and Wnt-2 induced growth alterations and signaling pathways in NIH3T3 fibroblasts

Anna Bafico, Arnona Gazit, Sidney S. Wu-Morgan, Abraham Yaniv, Stuart A. Aaronson*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

72 Scopus citations


Members of the Wnt family induce mouse mammary tumors and partially transform mammary epithelial cells in culture. However, their mechanism of transformation remains to be elucidated. In NIH3T3 mouse embryo fibroblasts, a standard transformation model, Wnt-1 and Wnt-2 were shown to induce altered properties including increased saturation density and growth in soft agar. Such cells also exhibited increased cell-cell adhesiveness. However, unlike oncogenes such as PDGFB or ras, Wnt-1 and -2 failed to induce detectable transformed foci following transfection, and stable NIH3T3 transfectants lacked tumor forming capacity. Wnt-1 and -2 transfectants exhibited increased uncomplexed, cytosolic β-catenin, which was not observed with PDGFB, ras or erbB2 transfectants. In transient transfection, Wnt-1 and -2 induced a rapid increase in cytosolic β-catenin but no detectable increase in the phosphorylated activated forms of MAP kinase. In contrast, ras was a potent activator of MAP kinase but had no effect on free β-catenin levels. These findings establish that both Wnt signaling and pattern of growth alterations differ from those of oncogenes which activate proliferative signaling pathways in NIH3T3 cells.

Original languageEnglish
Pages (from-to)2819-2825
Number of pages7
Issue number21
StatePublished - 28 May 1998


FundersFunder number
National Institutes of Health
National Cancer InstituteR01CA071672


    • Cell adhesion
    • MAPK
    • NIH3T3
    • Oncogene
    • Wnt
    • β-catenin


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