Аннотация:Obesity is a known risk factor for several cancers, with dysregulated cholesterol metabolism and altered adipokine signaling playing key roles in this association. T-cadherin (encoded by the CDH13 gene) is a cell surface receptor involved in mediating the effects of low-density lipoproteins (LDL) and adiponectin, two critical factors in obesity-related diseases. T-cadherin, lacking a transmembrane domain, is a unique molecular hub that both senses and modulates the effects of its ligands, regulating adipogenesis and lipid accumulation in adipose tissue. In this study, we explore the role of T-cadherin in adipocyte differentiation, using T-cadherin-deficient mice and mesenchymal stem cells (MSCs). We demonstrate that T-cadherin-deficient MSCs exhibit increased adipogenic differentiation and adipokine secretion, particularly adiponectin and leptin, while T-cadherin presence suppresses LDL-induced adipogenesis. Moreover, the downregulation of T-cadherin expression in various cancers suggests a potential tumor suppressor function, possibly through its involvement in adiponectin signaling and metabolic regulation. Our findings position T-cadherin as a crucial regulator linking obesity, adipose tissue homeostasis, and cancer progression, with implications for therapeutic targeting in obesity-related malignancies.