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© The Rockefeller University Press, 0021-9525/1999//855 $5.00
The Journal of Cell Biology, Volume 146, Number 4, , 1999 855-868

Original Article

Exogenous Expression of β-Catenin Regulates Contact Inhibition, Anchorage-Independent Growth, Anoikis, and Radiation-Induced Cell Cycle Arrest



Keith Orforda, Caroline C. Orforda, and Stephen W. Byersa

a The Lombardi Cancer Center and the Department of Cell Biology, Georgetown University School of Medicine, Washington, District of Columbia 20007
E415 The Research Building, GUMC, 3970 Reservoir Road N.W., Washington, DC 20007.(202) 687-7505(202) 687-1813

byerss{at}gunet.georgetown.edu

β-Catenin is an important regulator of cell–cell adhesion and embryonic development that associates with and regulates the function of the LEF/TCF family of transcription factors. Mutations of β-catenin and the tumor suppressor gene, adenomatous polyposis coli, occur in human cancers, but it is not known if, and by what mechanism, increased β-catenin causes cellular transformation. This study demonstrates that modest overexpression of β-catenin in a normal epithelial cell results in cellular transformation. These cells form colonies in soft agar, survive in suspension, and continue to proliferate at high cell density and following {gamma}-irradiation. Endogenous cytoplasmic β-catenin levels and signaling activity were also found to oscillate during the cell cycle. Taken together, these data demonstrate that β-catenin functions as an oncogene by promoting the G1 to S phase transition and protecting cells from suspension-induced apoptosis (anoikis).

Key Words: β-catenin • oncogene • cell cycle • anoikis • apoptosis

© 1999 The Rockefeller University Press

1.used in this paper: APC, adenomatous polyposis coli; CON, control; EMT, epithelial to mesenchymal transition; FAK, focal adhesion kinase; HA, hemagglutinin epitope; ILK, integrin-linked kinase; PKC, protein kinase C; S37A, S37A mutant β-catenin plasmid; WT, wild-type β-catenin plasmid


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