Beta 1-integrin–c-Met cooperation reveals an inside-in survival signalling on autophagy-related endomembranes View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2016-06-23

AUTHORS

Rachel Barrow-McGee, Naoki Kishi, Carine Joffre, Ludovic Ménard, Alexia Hervieu, Bakhouche A. Bakhouche, Alejandro J. Noval, Anja Mai, Camilo Guzmán, Luisa Robbez-Masson, Xavier Iturrioz, James Hulit, Caroline H. Brennan, Ian R. Hart, Peter J. Parker, Johanna Ivaska, Stéphanie Kermorgant

ABSTRACT

Receptor tyrosine kinases (RTKs) and integrins cooperate to stimulate cell migration and tumour metastasis. Here we report that an integrin influences signalling of an RTK, c-Met, from inside the cell, to promote anchorage-independent cell survival. Thus, c-Met and β1-integrin co-internalize and become progressively recruited on LC3B-positive 'autophagy-related endomembranes' (ARE). In cells growing in suspension, β1-integrin promotes sustained c-Met-dependent ERK1/2 phosphorylation on ARE. This signalling is dependent on ATG5 and Beclin1 but not on ATG13, suggesting ARE belong to a non-canonical autophagy pathway. This β1-integrin-dependent c-Met-sustained signalling on ARE supports anchorage-independent cell survival and growth, tumorigenesis, invasion and lung colonization in vivo. RTK-integrin cooperation has been assumed to occur at the plasma membrane requiring integrin 'inside-out' or 'outside-in' signalling. Our results report a novel mode of integrin-RTK cooperation, which we term 'inside-in signalling'. Targeting integrin signalling in addition to adhesion may have relevance for cancer therapy. More... »

PAGES

11942

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/ncomms11942

DOI

http://dx.doi.org/10.1038/ncomms11942

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1024256211

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/27336951


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