Introduction About E-cadherin (CDH1): Drug Target and Biomarker
Introduction About E-cadherin (CDH1): Drug Target and Biomarker
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.
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.
TH-TRalpha1 directly binds to the beta-catenin gene and increases its expression, while TRbeta-RXR complexes mediate CTNNB1 (beta-catenin) transrepression.
T3 can activate PKA to induce beta-catenin nuclear translocation, thereby modulating cyclin-D1 gene transcription and promoting cell proliferation.
E-cadherin-mediated cell-cell adhesion involves activation of the PI3K-Akt pathway, which influences membrane and actin dynamics, and reduces Rho activation.
E-cadherin downregulates receptor tyrosine kinase activation and stabilizes cell-cell contacts.
Pathogenic bacteria can cleave E-cadherin at specific sites, leading to the release of soluble extracellular E-cadherin fragments.
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.
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. These junctions play a role in suppressing the activation of the Wnt/beta-catenin pathway and the RTK/PI3K pathway in epithelial cells. E-cadherin expression promotes the extranuclear translocation of beta-catenin, suppressing the Wnt pathway.
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. This activation enhances cell survival and migration.
Additionally, the loss of E-cadherin expression has been associated with the acquisition of metastatic characteristics in breast cancer cells. 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.
Moreover, the cadherin-catenin complex at mature adherens junctions is involved in signaling events to the nucleus. 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. This binding can modulate the expression of specific target genes, including Wnt target genes.
Lastly, CDH1 (E-cadherin) plays a role in cell cycle regulation. Under normal conditions, CDH1 degrades SAG at the G1 phase but inhibits APC/C at the M phase, ensuring timely cell cycle progression. Alterations in SAG levels can disrupt this regulation and may lead to accelerated cell cycle progression, drug resistance, or aberrant mitotic progression.
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.
Protein Name: Cadherin 1
Functions: Cadherins are calcium-dependent cell adhesion proteins (PubMed:11976333). They preferentially interact with themselves in a homophilic manner in connecting cells; cadherins may thus contribute to the sorting of heterogeneous cell types. CDH1 is involved in mechanisms regulating cell-cell adhesions, mobility and proliferation of epithelial cells (PubMed:11976333). Has a potent invasive suppressor role. It is a ligand for integrin alpha-E/beta-7
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CDH10 | CDH11 | CDH12 | CDH13 | CDH13-AS2 | CDH15 | CDH16 | CDH17 | CDH18 | CDH19 | CDH2 | CDH20 | CDH22 | CDH23 | CDH24 | CDH26 | CDH3 | CDH4 | CDH5 | CDH6 | CDH7 | CDH8 | CDH9 | CDHR1 | CDHR18P | CDHR2 | CDHR3 | CDHR4 | CDHR5 | CDIN1 | CDIP1 | CDIPT | CDIPTOSP | CDK1 | CDK10 | CDK11A | CDK11B | CDK12 | CDK13 | CDK14 | CDK15 | CDK16 | CDK17 | CDK18 | CDK19 | CDK2 | CDK20 | CDK2AP1 | CDK2AP2 | CDK2AP2P2 | CDK2AP2P3 | CDK3 | CDK4 | CDK5 | CDK5R1 | CDK5R2 | CDK5RAP1 | CDK5RAP2 | CDK5RAP3 | CDK6 | CDK6-AS1 | CDK7 | CDK8 | CDK9 | CDKAL1 | CDKL1 | CDKL2 | CDKL3 | CDKL4 | CDKL5 | CDKN1A | CDKN1B | CDKN1C | CDKN2A | CDKN2A-DT | CDKN2AIP | CDKN2AIPNL | CDKN2AIPNLP1 | CDKN2B | CDKN2B-AS1 | CDKN2C | CDKN2D | CDKN3 | CDNF | CDO1 | CDON | CDPF1 | CDR1 | CDR2 | CDR2L | CDRT15 | CDRT15L2 | CDRT4 | CDRT7 | CDS1 | CDS2 | CDSN | CDT1 | CDV3 | CDX1
