Abstract
Cadherins play an important role in tissue homeostasis, as they are responsible for cell-cell adhesion during embryogenesis, tissue morphogenesis, differentiation and carcinogenesis. Cadherins are inseparably connected with catenins, forming cadherin-catenin complexes, which are crucial for cell-to-cell adherence. Any dysfunction or destabilization of cadherin-catenin complex may result in tumor progression. Epithelial mesenchymal transition (EMT) is a mechanism in which epithelial cadherin (E-cadherin) expression is lost during tumor progression. However, during tumorigenesis, many processes take place, and downregulation of E-cadherin, nuclear β-catenin and p120 catenin (p120) signaling are among the most critical. Additional signaling pathways, such as Receptor tyrosine kinase (RTK), Rho GTPases, phosphoinositide 3-kinase (PI3K) and Hippo affect cadherin cell-cell adhesion and also contribute to tumor progression and metastasis. Many signaling pathways may be activated during tumorigenesis; thus, cadherin-targeting drugs seem to limit the progression of malignant tumor. This review discusses the role of cadherins in selected signaling mechanisms involved in tumor growth. The clinical importance of cadherin will be discussed in cases of human and animal cancers.
Highlights
Cadherins are transmembrane glycoproteins responsible for cell-cell adhesion and maintenance of normal tissue architecture
The juxtamembrane domain of cadherin cytoplasmic tail binds to a family of proteins, including p120 catenin (p120; CTNND1), neural plakophilin-related armadillo protein (NPRAP/δ-catenin; CTNND2), armadillo repeat protein deleted in velo-cardio-facial syndrome (ARVCF) and plakophilin 4 (p0071)
Cadherins play an important role in tissue homeostasis and dysfunction
Summary
Cadherins are transmembrane glycoproteins responsible for cell-cell adhesion and maintenance of normal tissue architecture. The classical cadherins, among which there are many subgroups, are a class of adhesion molecules that interact with catenins through the cytoplasmic domain [1]. The five cadherins mediate Ca-dependent adhesion via their extracellular domains provide homotypic cell-cell interactions, and a cytoplasmic tail binds to several adaptor molecules to transmit physical and biochemical signals to the cell [6]. The role of cadherins in the process of cancer development has been studied widely over the last decades [6,10,11,12]. Recent studies have shown that E-cadherin, especially in late-stage cancers, may promote cell migration, invasion and even tumor progression [20,21,22,23,24]. The purpose of this review is to discuss the role of cadherins in the tumor growth and its clinical importance
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