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- W1985331569 abstract "The highly coordinated interaction of TGF-? and Wnt signaling pathways is critical for normal development. However, the effects of TGF-β on APC and beta-catenin, two key mediators of Wnt signaling in epithelial cells, have been largely unknown. We determined the effect of TGF-? on APC and beta-catenin expression in Mv1Lu, a non-transformed epithelial cell line, in which TGF-β signaling causes a G1 cell cycle arrest. We found that TGF-β rapidly reduced APC protein levels through a post-transcriptional mechanism. Further, TGF-beta increased beta-catenin mRNA and protein levels, and increased beta-catenin nuclear accumulation. Finally, retrovirus-mediated overexpression of beta-catenin discernibly enhanced the ability of TGF-β to induce a G1 cell cycle arrest. This is the first report demonstrating that TGF-β mimics the effect of Wnt signaling on beta-catenin in Mv1Lu cells, and that reduction of APC and nuclear accumulation of β-catenin have cooperative effects on mechanisms that mediate TGF-β-induced cell cycle arrest." @default.
- W1985331569 created "2016-06-24" @default.
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- W1985331569 date "2004-08-21" @default.
- W1985331569 modified "2023-10-17" @default.
- W1985331569 title "TGF-β Targets the Wnt Pathway Components, APC and β-catenin, as Mv1Lu Cells Undergo Cell Cycle Arrest" @default.
- W1985331569 doi "https://doi.org/10.4161/cc.3.8.1072" @default.
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