WNT/NFΚB CROSSTALK MAY DOWNREGULATE CYTOPLASMIC Β-CATENIN LEADING TO INDUCTION OF EMT.
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Author/Creator ORCID
Date
2018-04
Type of Work
Department
Biomedical and Environmental
Program
Biomedical Science
Citation of Original Publication
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Attribution-NonCommercial-ShareAlike 3.0 United States
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Abstract
Molecular interactions in the cell are not bound by discrete cellular pathways; there is significant communication between the pathways leading to tightly regulated processes. The current research will examine if Wnt and NFκB pathway component interplay can stimulate endothelial to mesenchymal transition (EMT) via the cell-junction component β-catenin (Ctnn-B). The classical Wnt pathway utilizes Ctnn-B as a signaling molecule; specifically, under activated canonical Wnt signaling to induce development. Cell-cell structure is maintained through various junctions, such as adherens junctions which utilize Ctnn-B to connect the cytoskeleton to E-cadherin, a transmembrane protein. Recently, a novel mechanism has been proposed wherein the NFκB pathway can also be inhibited by Ctnn-B. To determine adverse effects of Wnt/NFκB crosstalk on EMT, a previously developed Wnt signal sensor cell line was used to demonstrate five genes with changes in expression common to both Wnt and NFκB pathways. These genes will be silenced utilizing siRNA, after which a Wnt signal will be induced and western blotting will demonstrate any adverse alterations of Wnt/NFκB signaling capable of altering expression of Ctnn-B. Subsequent cell motility assays will demonstrate that Wnt/NFκB pathway alteration observed from western blotting can promote EMT to prove that pathway changes ultimately impact cellular physiology.