ITGB3-mediated uptake of small extracellular vesicles facilitates intercellular communication in breast cancer cells.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 32848136.
- Also identified by DOI 10.1038/s41467-020-18081-9 and PMC identifier 7450082.
- Licence recorded as CC BY.
- The licence permits redistribution, so the abstract is shown in full and the full text is available from the publisher.
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.
Medical subject headings
- Breast Neoplasms
- Cell Communication
- Extracellular Vesicles
- Integrin beta3