The E-Cadherin and N-Cadherin Switch in Epithelial-to-Mesenchymal Transition: Signaling, Therapeutic Implications, and Challenges

The E-Cadherin and N-Cadherin Switch in Epithelial-to-Mesenchymal Transition: Signaling, Therapeutic Implications, and Challenges

20 September 2019 | Chin-Yap Loh, Jian Yi Chai, Ting Fang Tang, Won Fen Wong, Gautam Sethi, Muthu Kumaraswamy Shanmugam, Pei Pei Chong, Chung Yeng Looi
The article reviews the role of E-cadherin and N-cadherin in epithelial-to-mesenchymal transition (EMT) and their significance in cancer progression. E-cadherin, a classical cadherin, is crucial for maintaining epithelial cell integrity and suppressing tumor growth, while N-cadherin is more prevalent in non-epithelial tissues and is associated with enhanced migratory and invasive traits in cancer cells. The "cadherin switch" during EMT involves the downregulation of E-cadherin and upregulation of N-cadherin, which is regulated by various signaling pathways such as Wnt/β-catenin, PI3K/AKT, TCF/LEF, and RhoA. These pathways are involved in modulating cell proliferation, migration, and invasion. The article also discusses the therapeutic implications of targeting EMT, including the use of shRNA, miRNA, small molecules, tyrosine kinase inhibitors, monoclonal antibodies, and natural compounds like curcumin. Natural compounds, particularly curcumin, have shown potential in inhibiting EMT and cancer progression by modulating signaling pathways and promoting apoptosis. The review highlights the challenges in translating these findings into clinical applications and emphasizes the need for further research to develop effective interventions for cancer treatment.The article reviews the role of E-cadherin and N-cadherin in epithelial-to-mesenchymal transition (EMT) and their significance in cancer progression. E-cadherin, a classical cadherin, is crucial for maintaining epithelial cell integrity and suppressing tumor growth, while N-cadherin is more prevalent in non-epithelial tissues and is associated with enhanced migratory and invasive traits in cancer cells. The "cadherin switch" during EMT involves the downregulation of E-cadherin and upregulation of N-cadherin, which is regulated by various signaling pathways such as Wnt/β-catenin, PI3K/AKT, TCF/LEF, and RhoA. These pathways are involved in modulating cell proliferation, migration, and invasion. The article also discusses the therapeutic implications of targeting EMT, including the use of shRNA, miRNA, small molecules, tyrosine kinase inhibitors, monoclonal antibodies, and natural compounds like curcumin. Natural compounds, particularly curcumin, have shown potential in inhibiting EMT and cancer progression by modulating signaling pathways and promoting apoptosis. The review highlights the challenges in translating these findings into clinical applications and emphasizes the need for further research to develop effective interventions for cancer treatment.
Reach us at info@study.space