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

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

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...

Full description

Saved in:
Bibliographic Details
Published in:The Journal of cell biology Vol. 146; no. 4; pp. 855 - 867
Main Authors: Orford, Keith, Orford, Caroline C., Byers, Stephen W.
Format: Journal Article
Language:English
Published: United States Rockefeller University Press 23-08-1999
The Rockefeller University Press
Subjects:
Animals
Apoptosis
B lymphocytes
beta Catenin
Cell adhesion
Cell Count - radiation effects
Cell cycle
Cell Cycle - radiation effects
Cell growth
Cell Line
Cell lines
Cell Size
Cell Transformation, Neoplastic - radiation effects
Cells
Cellular biology
Contact Inhibition - radiation effects
Cultured cells
Cytoskeletal Proteins - genetics
Cytoskeletal Proteins - physiology
Dogs
Epithelial cells
Gamma Rays
Gene Expression
Interphase
Interphase - radiation effects
Models, Biological
Mutation
Oncogenes - genetics
Oncogenes - physiology
Original
Recombinant Fusion Proteins - genetics
Recombinant Fusion Proteins - metabolism
Scientific imaging
Signal Transduction
Trans-Activators
Transgenes - genetics
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary: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).
Bibliography:ObjectType-Article-2
SourceType-Scholarly Journals-1
ObjectType-Feature-1
content type line 23
ObjectType-Article-1
ObjectType-Feature-2
ISSN:0021-9525
1540-8140
DOI:10.1083/jcb.146.4.855