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Cell and Tumor Biology |
1 Department of Biochemistry and Molecular Biology, Thoracic Diseases Research Unit, and Mayo Clinic Cancer Center, Mayo Clinic College of Medicine, Rochester, Minnesota and 2 Division of Basic Medical Sciences, Memorial University of Newfoundland, St. Johns, Newfoundland
Requests for reprints: Edward B. Leof, Stabile 8-58, Mayo Clinic, 200 First Street Southwest, Rochester, MN 55905. Phone: 507-284-5717; Fax: 507-284-4521; E-mail: leof.edward{at}mayo.edu.
Transforming growth factor-ß (TGF-ß) stimulates cellular proliferation and transformation to a myofibroblast phenotype in vivo and in a subset of fibroblast cell lines. As the Smad pathway is activated by TGF-ß in essentially all cell types, it is unlikely to be the sole mediator of cell type–specific outcomes to TGF-ß stimulation. In the current study, we determined that TGF-ß receptor signaling activates phosphatidylinositol 3-kinase (PI3K) in several fibroblast but not epithelial cultures independently of Smad2 and Smad3. PI3K activation occurs in the presence of dominant-negative dynamin and is required for p21-activated kinase-2 kinase activity and the increased proliferation and morphologic change induced by TGF-ß in vitro.
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