Epithelial-Mesenchymal Transition (EMT) is a process by which epithelial cells lose their polarity and acquire mesenchymal characteristics, enabling them to migrate and invade. This process is crucial in normal development, particularly in processes like gastrulation, neural crest formation, and mammary gland branching morphogenesis. EMT is also implicated in cancer progression, where it allows cancer cells to escape from the primary tumor and metastasize. In breast cancer, EMT is associated with poor clinical outcomes and tumor aggressiveness. EMT is driven by various signaling pathways and transcription factors, including TGF-β, Wnt/β-catenin, Snail, Slug, Twist, and Six1. These factors are also misexpressed in breast cancer, contributing to tumor progression. EMT is not always a complete transition, but rather a dynamic process that can occur in various contexts, including collective migration. In breast cancer, EMT is associated with the acquisition of invasive and motile properties, and with the development of a tumor-initiating cell phenotype. EMT also contributes to resistance to chemotherapy and evasion of the immune system. The reactivation of developmental pathways in cancer may provide new targets for therapy. The Msx2/Cripto pathway is also involved in mammary gland development and EMT in breast cancer. The E-cadherin repressors Snail, Slug, and Twist are also involved in EMT in breast cancer. These factors are misexpressed in breast cancer and contribute to tumor progression. Overall, EMT is a complex process that plays a critical role in both normal development and cancer progression.Epithelial-Mesenchymal Transition (EMT) is a process by which epithelial cells lose their polarity and acquire mesenchymal characteristics, enabling them to migrate and invade. This process is crucial in normal development, particularly in processes like gastrulation, neural crest formation, and mammary gland branching morphogenesis. EMT is also implicated in cancer progression, where it allows cancer cells to escape from the primary tumor and metastasize. In breast cancer, EMT is associated with poor clinical outcomes and tumor aggressiveness. EMT is driven by various signaling pathways and transcription factors, including TGF-β, Wnt/β-catenin, Snail, Slug, Twist, and Six1. These factors are also misexpressed in breast cancer, contributing to tumor progression. EMT is not always a complete transition, but rather a dynamic process that can occur in various contexts, including collective migration. In breast cancer, EMT is associated with the acquisition of invasive and motile properties, and with the development of a tumor-initiating cell phenotype. EMT also contributes to resistance to chemotherapy and evasion of the immune system. The reactivation of developmental pathways in cancer may provide new targets for therapy. The Msx2/Cripto pathway is also involved in mammary gland development and EMT in breast cancer. The E-cadherin repressors Snail, Slug, and Twist are also involved in EMT in breast cancer. These factors are misexpressed in breast cancer and contribute to tumor progression. Overall, EMT is a complex process that plays a critical role in both normal development and cancer progression.