CDH1

Overview

CDH1 encodes E-cadherin, a calcium-dependent cell adhesion protein that is a central component of adherens junctions in epithelial tissues. By mediating cell–cell adhesion, CDH1 helps maintain epithelial integrity, polarity, and barrier function. Loss or reduction of CDH1 expression is widely associated with epithelial-mesenchymal transition (EMT), increased motility, and invasive behavior in cancer, and it is also clinically important in hereditary cancer predisposition, particularly in CDH1-mutated patients undergoing prophylactic or therapeutic gastric surgery.

In biomedical research, CDH1 is frequently used as an epithelial marker and readout of EMT status. Changes in CDH1 expression are often interpreted alongside mesenchymal markers such as vimentin and N-cadherin, and with EMT-associated transcription factors including Snail, Slug, Zeb1, Twist, and ZEB2. In the recent studies summarized below, CDH1/E-cadherin was used primarily as a marker of epithelial differentiation, barrier integrity, and treatment response in cancer, kidney injury, and other disease models.

Focus of Latest Publications

Recent publications have examined CDH1 primarily in the context of cancer biology, inherited predisposition, and epithelial integrity. In urothelial bladder cancer, investigators evaluated CDH1 polymorphisms and haplotypes, together with genomic repetitive elements, to assess prognostic significance. In invasive lobular carcinoma, CDH1 loss was used to model a collagen-rich, matrix-dependent tumor state and to identify therapeutic vulnerabilities. In gastric cancer, CDH1-mutated patients were included in a surgical cohort comparing robot-assisted and laparoscopic total gastrectomy, reflecting the clinical relevance of CDH1 in hereditary gastric cancer management.

Several studies focused on CDH1 as E-cadherin and its relationship to epithelial-mesenchymal transition. In breast cancer models, carbonized nanogels suppressed metastatic behavior by increasing E-cadherin while decreasing N-cadherin and vimentin, consistent with inhibition of EMT-associated motility. In pancreatic ductal adenocarcinoma, Claudin-1 knockout restored E-cadherin expression and reduced proliferation, migration, and EMT, highlighting the broader importance of epithelial junctional proteins in maintaining tissue integrity. In liver cancer, TMEM45B-driven progression was associated with EMT changes that included altered E-cadherin expression, further underscoring CDH1-linked epithelial phenotypes in tumor aggressiveness.

Beyond oncology, CDH1 was also identified in a proteomic study of porcine epididymis exosomes, where S-acylated CDH1 was among caput-enriched proteins detected in exosomal cargo and implicated in long-distance trafficking during sperm maturation. In pediatric idiopathic steroid-sensitive nephrotic syndrome, E-cadherin injury was investigated alongside VE-cadherin injury as a potential marker of disease status, suggesting a role for cadherin damage in epithelial and endothelial dysfunction. Together, these publications portray CDH1 as a marker and mediator of cell-cell adhesion, EMT suppression, and tissue-specific pathology across cancer and nonmalignant disease settings.

Key Publications

NEWJul Injury to E- and VE-Cadherin in Paediatric Idiopathic Steroid-Sensitive Nephrotic Syndrome: Potential Markers of the Disease Status. (Nephrology (Carlton, Vic.), 2026, PMID 42366509): "This study aimed to explore the pathophysiology by examining E-cadherin injury, observed in atopic dermatitis, and VE-cadherin injury, associated with systemic edema formation."
NEWJun Interplay between CDH1 polymorphisms, haplotypes, and genomic repetitive elements in urothelial bladder cancer prognosis. (Molecular biology reports, 2026, PMID 42334742): "E-cadherin, an important regulator of cell-cell adhesion encoded by the CDH1 gene, is frequently downregulated during malignant progression, serving as a hallmark of invasiveness."
NEWJun The APC/C adaptor Cdh1 stabilizes STING to potentiate innate immune activation in renal cell carcinoma. (Science signaling, 2026, PMID 42335217): "Here, we explored its role in innate immune regulation and identified a noncanonical, degradation-independent function of Cdh1 in clear cell renal cell carcinoma (ccRCC) through its stabilization of the cytosolic double-stranded DNA (dsDNA) sensor STING."
May Cocktail-like alginate-derived carbonized nanogels with diverse moieties attenuate tumor metastasis via potential multi-pathway modulation. (International journal of biological macromolecules, 2026, PMID 42167427): "Alg-CNGs suppressed epithelial-mesenchymal transition in 4T1 triple-negative breast cancer cells by increasing E-cadherin and decreasing N-cadherin and vimentin, thereby attenuating EMT-associated motility as evidenced by reduced migration/invasion and marked perturbation of actin organization and adhesion-related dynamics."
May Robot-assisted versus laparoscopic total gastrectomy: a western high-volume tertiary referral center experience. (Journal of robotic surgery, 2026, PMID 42156604): "...for gastric cancer or prophylaxis in CDH1-mutated patients at Karolinska University Hospital (Stockholm, Sweden) from 1 January 2015 to 31 August 2025."
Apr Elevated TMEM45B expression promotes liver cancer progression and is associated with MET signaling activation. (Scientific reports, 2026, PMID 41998230): "EMT-related changes were examined by immunofluorescence staining of vimentin and E-cadherin."
Apr Integrated transcriptomic and functional characterization of Claudin-1 reveals its oncogenic and immunomodulatory roles in pancreatic ductal adenocarcinoma. (Tissue barriers, 2026, PMID 41978949): "Claudin-1 knockout markedly inhibited proliferation, migration, and EMT, evidenced by downregulation of Snail and Slug and restoration of E-cadherin expression."
Jun Comprehensive S-acylation profiling of the porcine epididymis and exosomes reveals a role in cargo sorting and long-distance trafficking. (Journal of proteomics, 2026, PMID 41864562): "Validation identified 5 caput-enriched S-acylated proteins, including evolutionarily conserved OCLN, CDH1, PDZK1, BAG5, and SCRN1, which were detected in S-acylated forms within caput-derived exosomes and cauda exosomes, but absent in cauda tissue."
May LOX Inhibition Disrupts a Collagen-Integrin-MYC Axis to Suppress Progression of Invasive Lobular Carcinoma. (Cancer research, 2026, PMID 41706704): "...the collagen-rich matrix dependency in ILC created by CDH1 loss."