The article discusses epithelial plasticity, focusing on the processes of epithelial-mesenchymal transition (EMT) and mesenchymal-epithelial transition (MET) in both embryonic development and cancer. During embryonic development, cells undergo EMT to become motile and migrate, then MET to differentiate into various tissues. In cancer, EMT is reactivated, allowing cancer cells to delaminate from primary tumors, metastasize, and form secondary tumors. MET is also crucial for the colonization of distant sites by cancer cells. The article highlights the importance of understanding these processes to develop better therapeutic strategies. The article outlines how EMT and MET are regulated by transcription factors, epigenetic changes, and microRNAs. It also discusses the role of cell plasticity in cancer progression, including the reactivation of developmental programs. The study emphasizes that EMT and MET are not simply "all or nothing" transitions, but can occur in partial forms, with cells exhibiting both epithelial and mesenchymal traits. The article also explores the relationship between EMT and stemness, noting that EMT can confer stem-like properties on cells, but the regulation of stemness is independent of epithelial plasticity. The article addresses the challenges in targeting EMT for cancer therapy, as inhibiting EMT may not always prevent metastasis and could even promote it in some cases. It also highlights the potential of targeting cancer stem cells (CSCs) as a promising therapeutic approach, while acknowledging that new CSCs can arise from non-stem cancer cells. The article concludes by emphasizing the need for improved therapeutic strategies that consider the complex and dynamic nature of epithelial plasticity in cancer.The article discusses epithelial plasticity, focusing on the processes of epithelial-mesenchymal transition (EMT) and mesenchymal-epithelial transition (MET) in both embryonic development and cancer. During embryonic development, cells undergo EMT to become motile and migrate, then MET to differentiate into various tissues. In cancer, EMT is reactivated, allowing cancer cells to delaminate from primary tumors, metastasize, and form secondary tumors. MET is also crucial for the colonization of distant sites by cancer cells. The article highlights the importance of understanding these processes to develop better therapeutic strategies. The article outlines how EMT and MET are regulated by transcription factors, epigenetic changes, and microRNAs. It also discusses the role of cell plasticity in cancer progression, including the reactivation of developmental programs. The study emphasizes that EMT and MET are not simply "all or nothing" transitions, but can occur in partial forms, with cells exhibiting both epithelial and mesenchymal traits. The article also explores the relationship between EMT and stemness, noting that EMT can confer stem-like properties on cells, but the regulation of stemness is independent of epithelial plasticity. The article addresses the challenges in targeting EMT for cancer therapy, as inhibiting EMT may not always prevent metastasis and could even promote it in some cases. It also highlights the potential of targeting cancer stem cells (CSCs) as a promising therapeutic approach, while acknowledging that new CSCs can arise from non-stem cancer cells. The article concludes by emphasizing the need for improved therapeutic strategies that consider the complex and dynamic nature of epithelial plasticity in cancer.