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Table 1 The characteristics of podosomes and invadopodia

From: Invadopodia in cancer metastasis: dynamics, regulation, and targeted therapies

Parameters/properties

Podosomes

Invadopodia

Cell type

Monocyte/macrophage lineage cells (macrophages, dendritic cells, bone marrow-derived osteoclasts), endothelial cells, smooth muscle cells, fibroblasts, neural crest cells

Cancer cells (such as breast cancer, cervical cancer, pancreatic cancer, lung cancer, squamous cell carcinoma, gastric cancer, colorectal cancer, liver cancer, bone cancer, and melanoma)

Size

Diameter: 0.5–1 µm,

Height: 0.5–0.8 µm

Diameters: 0.5–3 µm,

Height: 2–5 µm

Structure

F-actin-rich puncta consisting of core (F-actin, ARP2/3 complex, WASP, WIP, CDC42, cortactin, cofilin), Ring (β2 and β3 integrins, vinculin, paxillin, talin) and cap (crosslinked and bundled filaments)

F-actin-rich puncta consisting of core (F-actin, ARP2/3 complex, N-WASP, WIP, CDC42, cortactin, cofilin, Diaphanous-related-formins, dynamin 2, fascin, cysteine-rich protein 2, MT1-MMP, TKS5, MenaINV), Ring (β1 and β3 integrins, vinculin, paxillin, zyxin, ILK)

Main functions

Adhesion, Migration, Mechanosensation, Phagocytosis (macrophages)

ECM degradation, Mechanosensing

Relationship with diseases

Normal physiological migration (such as wound healing and immune surveillance). Abnormal activation may lead to chronic inflammation or fibrosis

Directly drive tumor metastasis and drug resistance, significantly associated with poor patient prognosis

Commonality

Dependent on actin dynamics assembly and Rho family GTPases (such as Cdc42, Rac1). Involved in cell-environment interactions

Share regulatory mechanisms with actin reorganization and Rho GTPases, both requiring localized membrane protrusion and the generation of mechanical forces