Аннотация: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 γ-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).
