Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2-3
pubmed:dateCreated
2011-1-31
pubmed:abstractText
Invadopodia are actin-rich, adhesive protrusions that extend into and remodel the extracellular matrix. They are associated with high levels of pericellular proteolysis and correlate with the invasive capacity of a variety of tumour cells. Invadopodia have, thus, been proposed to recapitulate key events of the metastatic process. Although our understanding of the patho-physiology of invadopodia is still in its infancy, the molecular components and signalling pathways leading to their formation have received increasing attention. Recent studies have revealed that diverse membrane polarized secretory and endo/exocytic trafficking pathways converge at these structures for the delivery, in a temporally controlled and spatially confined manner, of key proteolytic enzymes. Here, we will focus our attention on MT1-MMP, a paradigmatic metalloprotease that is primarily responsible for the proteolytic activity of invadopodia. We propose that the biosynthetic/secretory pathway might be critical for the polarized delivery of MT1-MMP to invadopodia that form as "default response" whenever cells have to deal with extracellular matrix (ECM) of variable composition and stiffness. Conversely, "inducible" endo/exocytic trafficking routes might primarily control the delivery of MT1-MMP to invadopodia when cells need to respond in a fast and transient manner to soluble motogenic factors, rather than the insoluble ECM.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1618-1298
pubmed:author
pubmed:copyrightInfo
Copyright © 2010 Elsevier GmbH. All rights reserved.
pubmed:issnType
Electronic
pubmed:volume
90
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
108-14
pubmed:meshHeading
pubmed:articleTitle
Secretory and endo/exocytic trafficking in invadopodia formation: the MT1-MMP paradigm.
pubmed:affiliation
IFOM, Fondazione Istituto FIRC di Oncologia Molecolare, Via Adamello 16, 20139 Milan, Italy.
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't