2026-06-14T03:40:39Zhttps://repisalud.isciii.es/rest/oai/requestoai:repisalud.isciii.es:20.500.12105/109132024-11-29T19:58:28Zcom_20.500.12105_2173com_20.500.12105_2051col_20.500.12105_19597
Repisalud
author
Fuentes, Pedro
author
Sesé, Marta
author
Guijarro, Pedro J
author
Emperador, Marta
author
Sánchez-Redondo, Sara
author
Hümmer, Stefan
author
Ramón Y Cajal, Santiago
author
Peinado Selgas, Hector
2020-09-01T10:20:28Z
2020-09-01T10:20:28Z
2020-08-26
Nat Commun. 2020;11(1):4261.
10.1038/s41467-020-18081-9
2041-1723
Nature communications
32848136
http://hdl.handle.net/20.500.12105/10913
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.
eng
ITGB3-mediated uptake of small extracellular vesicles facilitates intercellular communication in breast cancer cells.
journal article
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