Epithelial-mesenchymal transition (EMT) is a vital biological process in which epithelial cells transform into mesenchymal cells, gaining migratory and invasive capabilities. This reversible process plays a critical role in embryonic development, wound healing, fibrosis, and cancer metastasis. EMT is regulated by key signaling pathways, including TGF-β, Wnt, and Notch, and orchestrated by transcription factors like Snail and Twist. In cancer, EMT facilitates invasion, metastasis, and therapy resistance, marking it as a significant factor in tumor progression. EMT also contributes to cancer stem cell formation and immune evasion. The interplay between EMT and mesenchymal-to-epithelial transition (MET) underscores cellular plasticity in metastasis, where cells revert to epithelial states in secondary sites. Recent advances in targeting EMT therapeutically-such as inhibitors of TGF-β and EMT transcription factors-offer hope for reducing metastasis and improving treatment outcomes. This work explores the molecular mechanisms and clinical implications of EMT, emphasizing its dual roles in physiology and pathology.