ITGB3-mediated uptake of small extracellular vesicles facilitates intercellular communication in breast cancer cells

Abstract

Metastasis, the spread of malignant cells from a primary tumour to distant sites, causes 90% of cancer-related deaths. The integrin ITGB3 has been previously described to play an essential role in breast cancer metastasis, but the precise mechanisms remain undefined. We have now uncovered essential and thus far unknown roles of ITGB3 in vesicle uptake. The functional requirement for ITGB3 derives from its interactions with heparan sulfate proteoglycans (HSPGs) and the process of integrin endocytosis, allowing the capture of extracellular vesicles and their endocytosis-mediated internalization. Key for the function of ITGB3 is the interaction and activation of focal adhesion kinase (FAK), which is required for endocytosis of these vesicles. Thus, ITGB3 has a central role in intracellular communication via extracellular vesicles, proposed to be critical for cancer metastasis. The integrin ITGB3 has been described to play an essential role in breast cancer metastasis, but the precise mechanisms remain undefined. Here the authors describe thus far unknown roles of ITGB3 in the uptake of extracellular vesicles, required for colony growth of breast cancer cells

Document Type

Article

Language

English

Publisher

 

Related items

Ministerio de Economía y Competitividad PI14/01320

Ministerio de Economía y Competitividad RD12/0036/0057

Ministerio de Economía y Competitividad CB16/12/00363

Agència de Gestió d'Ajuts Universitaris i de Recerca 2014/SGR-1131

Instituto de Salud Carlos III PT17/0019

Nature communications ; Vol. 11 (august 2020)

Recommended citation

This citation was generated automatically.

Rights

open access

Aquest document està subjecte a una llicència d'ús Creative Commons. Es permet la reproducció total o parcial, la distribució, la comunicació pública de l'obra i la creació d'obres derivades, fins i tot amb finalitats comercials, sempre i quan es reconegui l'autoria de l'obra original.

https://creativecommons.org/licenses/by/4.0/

This item appears in the following Collection(s)