Regular ArticleTissue-Specific Expression of β-Catenin in Normal Mesenchyme and Uveal Melanomas and Its Effect on Invasiveness☆
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Plant-derived small molecule inhibitors as modulators of EMT pathway in cancer chemoprevention
2021, Studies in Natural Products ChemistryCitation Excerpt :Downregulation of E‐cadherin correlates with EMT in colon epithelial cells [34]. E-cadherin releases free β‐catenin in the cytoplasm during EMT which is a multifunctional protein subunit of the cadherin protein complex and acts as an intracellular signal transducer in the Wnt signaling pathway [35]. β‐catenin also functions as a critical downstream transcriptional activator in the Wnt signaling pathway in the nucleus functioning as a cofactor for transcription factors driving the gene expression of important cell cycle proteins, oncogenes, and proteases.
E-Cadherin negatively modulates δ-catenin-induced morphological changes and RhoA activity reduction by competing with p190RhoGEF for δ-catenin
2008, Biochemical and Biophysical Research Communicationsβ-Catenin can bind directly to CRM1 independently of adenomatous polyposis coli, which affects its nuclear localization and LEF-1/β-catenin-dependent gene expression
2008, Cell Biology InternationalCitation Excerpt :The nuclear-cytoplasmic levels of β-catenin NES1−, NES2−, NES3−, and NES4− were similar to that of the wild-type β-catenin coexpressed with CRM1 (Fig. 4B). The purity of these nuclear and cytoplasmic fractions was demonstrated by showing that endogenous β-catenin was found only in the cytoplasmic fraction because NIH 3T3 cells contain endogenous β-catenin in the cytoplasm (Kim et al., 1998). These results show that CRM1 affects the nuclear levels of β-catenin either via the conventional nuclear export machinery or through competition with APC.
APC and Oncogenic KRAS Are Synergistic in Enhancing Wnt Signaling in Intestinal Tumor Formation and Progression
2006, GastroenterologyCitation Excerpt :This induces a shift in β-catenin intracellular distribution by increasing the intracellular (Wnt signaling) pool. Moreover, increased tyrosine-phosphorylation of β-catenin has been associated with malignancy.42 Thus, tyrosine-phosphorylation of β-catenin, induced by KRASV12G, might be responsible for the observed nuclear accumulation of β-catenin and increased Wnt signaling.
Transforming growth factor β (TGFβ) signalling in palatal growth, apoptosis and epithelial mesenchymal transformation (EMT)
2004, Archives of Oral BiologyCitation Excerpt :On the other hand, DNSmad4 totally inhibits LEF1 activation and palatal EMT. It is evident from these results46,54 that stimulation of the LEF1 transcription factor by TGFβ3 involves both up-regulation of LEF1 mRNA and activation of the LEF1 transcription factor in the palates by Smad2 and 4. Without the TGFβ3 ligand, palatal EMT cannot be achieved by LEF1.
Elevated Hyaluronan Production Induces Mesenchymal and Transformed Properties in Epithelial Cells
2003, Journal of Biological ChemistryCitation Excerpt :Overexpression of β-catenin via stable transfection also induces anchorage-independent growth in MDCK cells (25), as reproduced here in Fig. 4. In addition, increased cytoplasmic β-catenin has been linked to invasiveness (42, 43); and accordingly, we found here that overexpression of β-catenin in MDCK cells increased their ability to invade reconstituted basement membrane (Fig. 5). To determine whether endogenous hyaluronan-cell interactions are important in these phenomena, we tested whether treatment with hyaluronan oligomers reverses the effects of HGF or β-catenin.
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R. LanzaR. LangerW. Chick
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