Epithelial plasticity, the ability of cells to reversibly change their phenotype, is a common feature in both embryonic and cancer cells. During embryonic development, cells undergo epithelial-to-mesenchymal transition (EMT) to migrate and form tissues, followed by mesenchymal-to-epithelial transition (MET) to differentiate into various cell types. Similarly, in cancer, EMT is reactivated when cancer cells delaminate from a primary tumor to metastasize, while MET is involved in the localization and proliferation of disseminated cancer cells. Both processes highlight the importance of cell plasticity in development and cancer progression. EMT is triggered by extracellular signals, including TGFβ/BMP, Wnt, Notch, and others, leading to the activation of transcription factors (EMT-TFs) that repress epithelial traits and promote mesenchymal characteristics. These factors also influence cell survival, migration, and invasion. MET, the reverse process, is associated with the reversion to an epithelial phenotype and increased cell proliferation, essential for secondary tumor formation. Epigenetic, splicing, and microRNA networks regulate EMT and MET, contributing to cell plasticity. In cancer, EMT and MET are linked to stemness and metastasis. However, the relationship between EMT and stemness remains controversial. Some studies suggest that EMT can confer stem-like properties, while others indicate that MET is necessary for the reversion to an epithelial state. The interplay between EMT and stemness is complex, with EMT-TFs playing a key role in both processes. Targeting EMT and stem cells is a promising approach for cancer therapy. Inhibiting EMT may be counterproductive in tumors that disseminate early, as it could favor the formation of secondary tumors. Instead, strategies targeting cancer stem cells (CSCs) are being explored, as CSCs can initiate and maintain tumors. However, new CSCs can arise from differentiated tumor cells, highlighting the need for comprehensive therapeutic approaches. Recent advances in understanding EMT and MET have led to the identification of regulatory networks, including microRNAs, that control these processes. These insights are crucial for developing improved therapeutic strategies to combat cancer metastasis. The study of EMT and MET in both embryonic development and cancer provides valuable clues for understanding tumor progression and designing effective treatments.Epithelial plasticity, the ability of cells to reversibly change their phenotype, is a common feature in both embryonic and cancer cells. During embryonic development, cells undergo epithelial-to-mesenchymal transition (EMT) to migrate and form tissues, followed by mesenchymal-to-epithelial transition (MET) to differentiate into various cell types. Similarly, in cancer, EMT is reactivated when cancer cells delaminate from a primary tumor to metastasize, while MET is involved in the localization and proliferation of disseminated cancer cells. Both processes highlight the importance of cell plasticity in development and cancer progression. EMT is triggered by extracellular signals, including TGFβ/BMP, Wnt, Notch, and others, leading to the activation of transcription factors (EMT-TFs) that repress epithelial traits and promote mesenchymal characteristics. These factors also influence cell survival, migration, and invasion. MET, the reverse process, is associated with the reversion to an epithelial phenotype and increased cell proliferation, essential for secondary tumor formation. Epigenetic, splicing, and microRNA networks regulate EMT and MET, contributing to cell plasticity. In cancer, EMT and MET are linked to stemness and metastasis. However, the relationship between EMT and stemness remains controversial. Some studies suggest that EMT can confer stem-like properties, while others indicate that MET is necessary for the reversion to an epithelial state. The interplay between EMT and stemness is complex, with EMT-TFs playing a key role in both processes. Targeting EMT and stem cells is a promising approach for cancer therapy. Inhibiting EMT may be counterproductive in tumors that disseminate early, as it could favor the formation of secondary tumors. Instead, strategies targeting cancer stem cells (CSCs) are being explored, as CSCs can initiate and maintain tumors. However, new CSCs can arise from differentiated tumor cells, highlighting the need for comprehensive therapeutic approaches. Recent advances in understanding EMT and MET have led to the identification of regulatory networks, including microRNAs, that control these processes. These insights are crucial for developing improved therapeutic strategies to combat cancer metastasis. The study of EMT and MET in both embryonic development and cancer provides valuable clues for understanding tumor progression and designing effective treatments.