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.