Adherens junction (AJ)

Adherens junctions (AJs) are specialized cell-cell adhesion complexes that provide mechanical stability to tissues and coordinate vital intracellular signaling pathways [Wikipedia: Adherens junction; StatPearls: Physiology, Cell Junction]. These junctions are primarily composed of transmembrane cadherins, such as E-cadherin, which mediate calcium-dependent homophilic binding between adjacent cells, and cytoplasmic catenins (alpha, beta, and p120) that link the complex to the actin cytoskeleton [Nature Reviews Molecular Cell Biology: Adherens junctions in development and homeostasis]. Beyond their structural role, AJs act as hubs for signal transduction, influencing cell proliferation, polarity, and survival via pathways like Wnt/beta-catenin and Hippo [NCBI: PMC22898409]. In pathological contexts, particularly cancer, the loss of AJ integrity—often termed the 'cadherin switch'—is a fundamental driver of the epithelial-mesenchymal transition (EMT), allowing tumor cells to invade and metastasize [PubMed: 22898409]. Additionally, disruption of endothelial adherens junctions leads to increased vascular permeability and is implicated in inflammatory diseases and the breakdown of physiological barriers like the blood-brain barrier [PubMed: 30107773]. Therapeutic development focuses on targeting specific AJ components, including cadherin-blocking peptides like ADH-1 (Exherin) for cancer treatment and beta-catenin inhibitors like Tegavivint to suppress oncogenic signaling [ClinicalTrials.gov: NCT04851119; PubMed: 2910793].

Other names

Zonula adherensIntermediate junctionBelt desmosomeCell-cell adhesion complex

Inhibition of cadherin-mediated extracellular binding [PubMed: 2910793]; antagonism of beta-catenin-dependent transcriptional signaling [ClinicalTrials.gov: NCT04851119]; stabilization of cell-cell contacts to maintain barrier integrity [PubMed: 30107773].