Invadopodia: at the cutting edge of tumour invasion.
Invasion of tissues by malignant tumours is facilitated by tumour cell migration and degradation of extracellular matrix (ECM) barriers. Several invasive neoplasms, including head and neck squamous cell carcinoma, breast carcinoma, melanoma and glioma, contain tumour cells that can form actin-rich protrusions with ECM proteolytic activity called invadopodia. These dynamic organelle-like structures adhere to, and digest, collagens, laminins and fibronectin. Invadopodia are dependent on multiple transmembrane, cytoplasmic and secreted proteins engaged in cell adhesion, signal transduction, actin assembly, membrane regulation and ECM proteolysis. Strategies aimed at disrupting invadopodia could form the basis of novel anti-invasive therapies for treating patients. Here we review the molecular basis of invadopodia formation with particular emphasis on the intracellular signaling networks that are essential for invadopodia activity and examine the potential role of these structures in glioma invasion.
Stylli
Stanley S
SS
Department of Surgery, University of Melbourne, Cell Signaling Laboratory, Level 5, Clinical Sciences Building, Royal Melbourne Hospital, Parkville, Victoria 3050, Australia.
Kaye
Andrew H
AH
Lock
Peter
P
D001932:Brain Neoplasms / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D002448:Cell Adhesion; D022081:Cell Surface Extensions / Q000378:metabolism* / Q000648:ultrastructure; D005109:Extracellular Matrix / Q000378:metabolism*; D016326:Extracellular Matrix Proteins / Q000378:metabolism; D005910:Glioma / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D006801:Humans; D009361:Neoplasm Invasiveness / Q000473:pathology / Q000503:physiopathology*; D009369:Neoplasms / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D015398:Signal Transduction
D016326:Extracellular Matrix Proteins