AI Article Synopsis
- E-cadherin is crucial for the formation and maintenance of epithelial tissues, especially in the colon, where it creates a barrier essential for organ homeostasis.
- Compromised E-cadherin function can lead to issues like inflammation and contribute to colon cancer development.
- Recent research has uncovered new roles for E-cadherin in cell signaling that can promote tumor growth, suggesting a complex relationship between E-cadherin and colon tumorigenesis.
Article Abstract
E-cadherin is the core component of epithelial adherens junctions, essential for tissue development, differentiation, and maintenance. It is also fundamental for tissue barrier formation, a critical function of epithelial tissues. The colon or large intestine is lined by an epithelial monolayer that encompasses an E-cadherin-dependent barrier, critical for the homeostasis of the organ. Compromised barriers of the colonic epithelium lead to inflammation, fibrosis, and are commonly observed in colorectal cancer. In addition to its architectural role, E-cadherin is also considered a tumor suppressor in the colon, primarily a result of its opposing function to Wnt signaling, the predominant driver of colon tumorigenesis. Beyond these well-established traditional roles, several studies have portrayed an evolving role of E-cadherin as a signaling epicenter that regulates cell behavior in response to intra- and extra-cellular cues. Intriguingly, these recent findings also reveal tumor-promoting functions of E-cadherin in colon tumorigenesis and new interacting partners, opening future avenues of investigation. In this Review, we focus on these emerging aspects of E-cadherin signaling, and we discuss their implications in colon biology and disease.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6600153 | PMC |
| http://dx.doi.org/10.3390/ijms20112756 | DOI Listing |
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