The epithelial-mesenchymal transition (EMT) is a process where epithelial cells lose their polarity and adhesion, reorganize their cytoskeleton, and acquire mesenchymal characteristics, which is crucial in development, wound healing, and cancer progression. This process is mediated by key transcription factors such as SNAIL, ZEB, and basic helix-loop-helix (bHLH) factors, which regulate gene expression and signaling pathways. EMT is characterized by the downregulation of epithelial genes like E-cadherin and the upregulation of mesenchymal genes, leading to increased cell motility and invasiveness. The process involves the dissolution of cell junctions, loss of apical-basal polarity, and reorganization of the cytoskeleton. Signaling pathways such as TGFβ, WNT, and Notch play critical roles in EMT, with TGFβ being a major driver. EMT is also involved in the reversal process, mesenchymal-epithelial transition (MET), and is essential for stem cell behavior and tissue regeneration. The molecular mechanisms of EMT include changes in gene expression, cytoskeletal reorganization, and the regulation of cell junctions and polarity. Transcription factors like SNAIL, TWIST, and ZEB regulate EMT by modulating gene expression and interacting with other signaling pathways. Additionally, non-coding miRNAs and alternative splicing of mRNAs contribute to the regulation of EMT. The TGFβ signaling pathway, through SMADs, plays a central role in EMT, with SMAD2, SMAD3, and SMAD4 being key regulators. Other signaling pathways, such as PI3K-AKT and ERK MAPK, also contribute to EMT by modulating gene expression and cell behavior. Growth factors and FGF signaling can also induce EMT, highlighting the complexity of the molecular mechanisms underlying this process.The epithelial-mesenchymal transition (EMT) is a process where epithelial cells lose their polarity and adhesion, reorganize their cytoskeleton, and acquire mesenchymal characteristics, which is crucial in development, wound healing, and cancer progression. This process is mediated by key transcription factors such as SNAIL, ZEB, and basic helix-loop-helix (bHLH) factors, which regulate gene expression and signaling pathways. EMT is characterized by the downregulation of epithelial genes like E-cadherin and the upregulation of mesenchymal genes, leading to increased cell motility and invasiveness. The process involves the dissolution of cell junctions, loss of apical-basal polarity, and reorganization of the cytoskeleton. Signaling pathways such as TGFβ, WNT, and Notch play critical roles in EMT, with TGFβ being a major driver. EMT is also involved in the reversal process, mesenchymal-epithelial transition (MET), and is essential for stem cell behavior and tissue regeneration. The molecular mechanisms of EMT include changes in gene expression, cytoskeletal reorganization, and the regulation of cell junctions and polarity. Transcription factors like SNAIL, TWIST, and ZEB regulate EMT by modulating gene expression and interacting with other signaling pathways. Additionally, non-coding miRNAs and alternative splicing of mRNAs contribute to the regulation of EMT. The TGFβ signaling pathway, through SMADs, plays a central role in EMT, with SMAD2, SMAD3, and SMAD4 being key regulators. Other signaling pathways, such as PI3K-AKT and ERK MAPK, also contribute to EMT by modulating gene expression and cell behavior. Growth factors and FGF signaling can also induce EMT, highlighting the complexity of the molecular mechanisms underlying this process.