The epithelial–mesenchymal transition (EMT) is a process that transforms epithelial cells into mesenchymal cells, enabling them to acquire traits associated with metastasis. EMT is orchestrated by transcription factors (TFs) that repress epithelial adhesion and promote mesenchymal features. These TFs are crucial for the early steps of metastasis, including local invasion and dissemination of cancer cells. However, the subsequent colonization of distant tissues by micrometastatic cells is also linked to the self-renewal properties of cancer stem cells (CSCs), which are essential for tumor growth and recurrence. EMT programs are closely associated with the acquisition of CSC traits, as they can induce self-renewal and stemness in cancer cells. Molecular links between EMT-TFs and self-renewal have been identified, suggesting that EMT plays a critical role in both early and late stages of the metastatic cascade. The genetic and epigenetic mechanisms regulating EMT-TFs and their effects are areas of active research, with potential implications for therapeutic strategies targeting CSCs and overcoming tumor heterogeneity and resistance. EMT is also linked to the regulation of stem-cell states, with factors such as Wnt-beta-catenin signaling playing a key role in maintaining stemness. The interplay between EMT and CSCs highlights the importance of targeting these processes to develop effective therapies for cancer.The epithelial–mesenchymal transition (EMT) is a process that transforms epithelial cells into mesenchymal cells, enabling them to acquire traits associated with metastasis. EMT is orchestrated by transcription factors (TFs) that repress epithelial adhesion and promote mesenchymal features. These TFs are crucial for the early steps of metastasis, including local invasion and dissemination of cancer cells. However, the subsequent colonization of distant tissues by micrometastatic cells is also linked to the self-renewal properties of cancer stem cells (CSCs), which are essential for tumor growth and recurrence. EMT programs are closely associated with the acquisition of CSC traits, as they can induce self-renewal and stemness in cancer cells. Molecular links between EMT-TFs and self-renewal have been identified, suggesting that EMT plays a critical role in both early and late stages of the metastatic cascade. The genetic and epigenetic mechanisms regulating EMT-TFs and their effects are areas of active research, with potential implications for therapeutic strategies targeting CSCs and overcoming tumor heterogeneity and resistance. EMT is also linked to the regulation of stem-cell states, with factors such as Wnt-beta-catenin signaling playing a key role in maintaining stemness. The interplay between EMT and CSCs highlights the importance of targeting these processes to develop effective therapies for cancer.