Review highlights multifaceted signaling pathways of T-cadherin across mammalian systems, indicating its critical involvement in cancer, metabolism, and cardiovascular disease.
T-cadherin is a cadherin and cell adhesion molecule that is anchored to the cell surface membrane through a glycosylphosphatidylinositol moiety. T-cadherin lacks a transmembrane and cytoskeletal domain, suggesting that it must interact with other membrane-bound molecules to elicit cellular signaling to modulate normal cellular functions, and alternatively its absence can be a factor in promoting neoplasia. Moreover, apart from binding to itself it can sequester adiponectin to the cell surface. Consistent with these observations, recent research has expanded the scope of T-cadherin’s role in cancer, neuronal function, metabolism and cardiovascular disease. In this context, we highlight the experimental and genomic evidence that links T-cadherin with these diseases. In particular, we discuss how T-cadherin homophilic and heterophilic interactions impact on signaling pathways and cellular behavior.
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Sternberg et al. (2017) studied this question.
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