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Differentiation of Mouse Breast Epithelial HC11 and EpH4 Cells
Published on: February 27, 2020
Membrane Bound E-Cadherin Stimulates PI3K/Akt Signaling
Aurora Candelario-Martínez1, Mónica Vizcarra-Soto2, Nicolás Villegas-Sepúlveda2
1Department of Physiology, Biophysics and Neurosciences, CINVESTAV IPN, Mexico City, México.
Abstract:
Cell junction proteins play a pivotal role in regulating key physiological processes, including proliferation and apoptosis. E-cadherin, a crucial component of adherens junctions, is essential for maintaining intestinal epithelial homeostasis by modulating cell adhesion and proliferation. In this study, we explored the function of E-cadherin in the intestinal epithelial cells. Our findings indicate that during colitis, E-cadherin remains associated with the cell membrane in colonocytes. Furthermore, using an in vitro system, we demonstrated that in colonocytes, E-cadherin inhibits cell proliferation and β-catenin signaling while simultaneously activating the PI3K/Akt pathway. These results suggest that E-cadherin may suppress cell proliferation while promoting PI3K/Akt signaling in colonocytes of colitic mice.
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