Epithelial–mesenchymal transition (EMT) plays a critical role in promoting tumor metastasis in epithelial-derived carcinomas. EMT involves the loss of epithelial characteristics and gain of mesenchymal traits, enabling cancer cells to invade, intravasate, and metastasize. The reverse process, mesenchymal–epithelial transition (MET), allows cancer cells to re-establish epithelial characteristics for colonization. EMT is regulated by transcription factors such as Snail, Zeb, and Twist, which repress epithelial markers like E-cadherin and promote mesenchymal markers like vimentin. EMT is induced by various signals, including TGF-β, Wnt, and hypoxia, and is essential for tumor cell migration, invasion, and survival in the bloodstream. EMT also contributes to drug resistance and cancer stem cell (CSC) formation, which are critical for metastasis and recurrence. Clinical evidence shows that EMT markers are present in circulating tumor cells (CTCs) and are associated with poor prognosis. Targeting EMT and MET could be a promising strategy for treating metastatic cancers. However, current therapies are limited in their ability to target EMT cells, and further research is needed to understand the molecular mechanisms and develop effective therapeutic approaches.Epithelial–mesenchymal transition (EMT) plays a critical role in promoting tumor metastasis in epithelial-derived carcinomas. EMT involves the loss of epithelial characteristics and gain of mesenchymal traits, enabling cancer cells to invade, intravasate, and metastasize. The reverse process, mesenchymal–epithelial transition (MET), allows cancer cells to re-establish epithelial characteristics for colonization. EMT is regulated by transcription factors such as Snail, Zeb, and Twist, which repress epithelial markers like E-cadherin and promote mesenchymal markers like vimentin. EMT is induced by various signals, including TGF-β, Wnt, and hypoxia, and is essential for tumor cell migration, invasion, and survival in the bloodstream. EMT also contributes to drug resistance and cancer stem cell (CSC) formation, which are critical for metastasis and recurrence. Clinical evidence shows that EMT markers are present in circulating tumor cells (CTCs) and are associated with poor prognosis. Targeting EMT and MET could be a promising strategy for treating metastatic cancers. However, current therapies are limited in their ability to target EMT cells, and further research is needed to understand the molecular mechanisms and develop effective therapeutic approaches.