Podosomes and invadopodia are dynamic actin-based structures in metazoan cells that serve as sites of ECM attachment and degradation. They are found in various cell types, including cancer cells, vascular smooth muscle cells, endothelial cells, and immune cells. Recent research has advanced understanding of their regulatory mechanisms and roles in disease. Podosomes are typically found in normal cells, while invadopodia are associated with cancer cells. However, the original discovery of these structures in Src-transformed cells suggests they may be functionally similar. The terms 'podosome' and 'invadopodia' are used to distinguish structures based on cell type, with invadopodia being more associated with ECM degradation and cell migration in cancer cells. Both structures are composed of an actin-rich core surrounded by adhesion and scaffolding proteins. Key components include cortactin, (N)-WASP, Tks4, Tks5, Src, and MT1-MMP. While podosomes and invadopodia share many components, they differ in morphology and function. Invadopodia are more stable and have a greater capacity for ECM degradation, which is crucial for cancer cell invasion and metastasis. Podosomes are more transient and involved in cell migration. The formation and function of podosomes and invadopodia are regulated by various signaling pathways, including those involving Src, PKC, integrins, and reactive oxygen species (ROS). MicroRNAs also play a role in regulating podosome formation. The assembly and turnover of these structures are tightly controlled, with podosomes and invadopodia playing roles in cell migration, ECM remodeling, and disease progression. In vivo, podosomes and invadopodia are involved in physiological processes such as bone resorption and vascular homeostasis. Mutations in podosome-associated proteins can lead to genetic disorders like Frank-ter-Haar syndrome. In cancer, podosomes and invadopodia contribute to tumor progression and metastasis by facilitating ECM degradation and cell migration. Understanding the regulation and function of these structures is crucial for developing therapeutic strategies targeting cancer and other diseases.Podosomes and invadopodia are dynamic actin-based structures in metazoan cells that serve as sites of ECM attachment and degradation. They are found in various cell types, including cancer cells, vascular smooth muscle cells, endothelial cells, and immune cells. Recent research has advanced understanding of their regulatory mechanisms and roles in disease. Podosomes are typically found in normal cells, while invadopodia are associated with cancer cells. However, the original discovery of these structures in Src-transformed cells suggests they may be functionally similar. The terms 'podosome' and 'invadopodia' are used to distinguish structures based on cell type, with invadopodia being more associated with ECM degradation and cell migration in cancer cells. Both structures are composed of an actin-rich core surrounded by adhesion and scaffolding proteins. Key components include cortactin, (N)-WASP, Tks4, Tks5, Src, and MT1-MMP. While podosomes and invadopodia share many components, they differ in morphology and function. Invadopodia are more stable and have a greater capacity for ECM degradation, which is crucial for cancer cell invasion and metastasis. Podosomes are more transient and involved in cell migration. The formation and function of podosomes and invadopodia are regulated by various signaling pathways, including those involving Src, PKC, integrins, and reactive oxygen species (ROS). MicroRNAs also play a role in regulating podosome formation. The assembly and turnover of these structures are tightly controlled, with podosomes and invadopodia playing roles in cell migration, ECM remodeling, and disease progression. In vivo, podosomes and invadopodia are involved in physiological processes such as bone resorption and vascular homeostasis. Mutations in podosome-associated proteins can lead to genetic disorders like Frank-ter-Haar syndrome. In cancer, podosomes and invadopodia contribute to tumor progression and metastasis by facilitating ECM degradation and cell migration. Understanding the regulation and function of these structures is crucial for developing therapeutic strategies targeting cancer and other diseases.