CDH1 Target Analysis Report Summary
About the Target
Based on the given context information, the following key viewpoints can be extracted regarding E-cadherin (CDH1):
E-cadherin plays a crucial role in cell-cell adhesion and is involved in the regulation of cell proliferation, differentiation, and apoptosis in gastrointestinal epithelial cells [1].
The transcription of E-cadherin, beta-catenin, and alpha-catenin genes can be activated by T3 (thyroid hormone) in differentiating epithelial cells, promoting cell differentiation and reducing the oncogenic effects [1].
TH-TRalpha1 directly binds to the beta-catenin gene and increases its expression, while TRbeta-RXR complexes mediate CTNNB1 (beta-catenin) transrepression [1].
T3 can activate PKA to induce beta-catenin nuclear translocation, thereby modulating cyclin-D1 gene transcription and promoting cell proliferation [2].
E-cadherin-mediated cell-cell adhesion involves activation of the PI3K-Akt pathway, which influences membrane and actin dynamics, and reduces Rho activation [3].
E-cadherin downregulates receptor tyrosine kinase activation and stabilizes cell-cell contacts [3].
Pathogenic bacteria can cleave E-cadherin at specific sites, leading to the release of soluble extracellular E-cadherin fragments [4].
The Rho/ROCK/E-cadherin cascade and Galphai/o and Galpha11/q-dependent signaling cascades are involved in mediating the effects of LPA (lysophosphatidic acid) on cell motility, with the Rho/ROCK pathway being the predominant pathway [5].
Overall, E-cadherin is essential for cell-cell adhesion and is regulated by various signaling pathways. Its expression and function are influenced by thyroid hormones and can impact cell proliferation, differentiation, and apoptosis. E-cadherin also plays a role in maintaining cell-cell contacts and modulating cell motility.
Based on the given context information, the keyword "E-cadherin" (synonymous with CDH1) is associated with several important functions and signaling pathways in cell adhesion and regulation.
Firstly, E-cadherin forms stable adherens junctions, enabling strong cell-to-cell contact [6]. These junctions play a role in suppressing the activation of the Wnt/beta-catenin pathway and the RTK/PI3K pathway in epithelial cells [6]. E-cadherin expression promotes the extranuclear translocation of beta-catenin, suppressing the Wnt pathway [6].
In non-epithelial cells, N-cadherin-mediated adherens junctions facilitate cell survival and migration by activating the MAPK/ERK pathway and the PI3K pathway in association with PDGFR [6]. This activation enhances cell survival and migration [6].
Additionally, the loss of E-cadherin expression has been associated with the acquisition of metastatic characteristics in breast cancer cells [7]. Distinct complexes called Ring1b complexes can cause epigenetic changes on the E-cadherin promoter, leading to the silencing of E-cadherin and the acquisition of metastatic properties [7].
Moreover, the cadherin-catenin complex at mature adherens junctions is involved in signaling events to the nucleus [8]. In conditions that alter E-cadherin-mediated adhesion, such as phosphorylation, endocytosis, or loss of E-cadherin expression, beta-catenin and p120 can bind their nuclear effectors [8]. This binding can modulate the expression of specific target genes, including Wnt target genes [8].
Lastly, CDH1 (E-cadherin) plays a role in cell cycle regulation [9]. Under normal conditions, CDH1 degrades SAG at the G1 phase but inhibits APC/C at the M phase, ensuring timely cell cycle progression [9]. Alterations in SAG levels can disrupt this regulation and may lead to accelerated cell cycle progression, drug resistance, or aberrant mitotic progression [9].
In summary, E-cadherin, or CDH1, is involved in cell adhesion, regulation of signaling pathways (such as Wnt/beta-catenin and RTK/PI3K), acquisition of metastatic properties, regulation of target gene expression, and cell cycle progression.
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Note: If you are interested in the full version of this target analysis report, or if you'd like to learn how our AI-powered BDE-Chem can design therapeutic molecules to interact with the CDH1 target at a cost 90% lower than traditional approaches, please feel free to contact us at BD@silexon.ai.
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