E-Cadherin and its signaling pathways: A novel target of dietary components in modulating cell migration and proliferation.

E-cadherin plays a critical role in preserving cell-cell adhesion and tissue integrity, and its reduced expression is a hallmark feature of the epithelial-mesenchymal transition (EMT) associated with cancer metastasis. This paper explores signaling pathways, including Snail family transcriptional repressor (Snail), Mitogen-activated protein kinase (MAPK), Store-operated calcium entry (SOCE), Transforming growth factor (TGF-β), Janus kinase/signal transducers and activators of transcription (JAK/STAT), Wingless-related integration site (Wnt), and Renin angiotensin system (RAS), elucidating their functions in regulating E-cadherin levels and controlling cell migration and proliferation. Also, regulation of E-cadherin signaling pathways by various dietary components is explored. This comprehensive review presents the critical role of E-cadherin and its associated pathways in various diseases, particularly cancer and cardiovascular conditions. Additionally, the article discusses the influence of dietary components like antioxidants, polyphenols, and herbs on E-cadherin pathways, offering potential pathways for modulating cell migration and proliferation in chronic diseases. It emphasizes the potential for therapeutic interventions targeting these pathways and suggests the significance of considering dietary factors in disease prevention and treatment strategies. • Loss of E-cadherin is an essential element of invasion and metastasis. • E-cadherin and related pathways including Snail, MAPK, SOCE, TGF-β, JAK/STAT, Wnt, and RAS regulate migration and proliferation. • Dietary components influence the E-cadherin pathways and interaction. [ABSTRACT FROM AUTHOR]