Homosalate boosts the release of tumour‐derived extracellular vesicles with protection against anchorage‐loss property
Abstract
Eukaryotic cells, including cancer cells, secrete highly heterogeneous populations of extracellular vesicles (EVs). EVs could have different subcellular origin, composition and functional properties, but tools to distinguish between EV subtypes are scarce. Here, we tagged CD63- or CD9-positive EVs secreted by triple negative breast cancer cells with Nanoluciferase enzyme, to set-up a miniaturized method to quantify secretion of these two EV subtypes directly in the supernatant of cells. We performed a cell-based high-content screening to identify clinically-approved drugs able to affect EV secretion. One of the identified hits is Homosalate, an anti-inflammatory drug found in sunscreens which robustly increased EVs' release. Comparing EVs induced by Homosalate with those induced by Bafilomycin A1, we demonstrate that: (1) the two drugs act on EVs generated in distinct subcellular compartments, and (2) EVs released by Homosalate-, but not by Bafilomycin A1-treated cells enhance resistance to anchorage loss in another recipient epithelial tumour cell line. In conclusion, we identified a new drug modifying EV release and demonstrated that under influence of different drugs, triple negative breast cancer cells release EV subpopulations from different subcellular origins harbouring distinct functional properties.
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BibTeX
@article{grisard2026homosalate,
title = {{Homosalate boosts the release of tumour‐derived extracellular vesicles with protection against anchorage‐loss property}},
author = {Eleonora Grisard and Nathalie Nevo and Aurianne Lescure and Sebastian Doll and Maxime Corbé and Mabel Jouve and Gregory Lavieu and Alain Joliot and Elaine Del Nery and Lorena Martin-Jaular and Clotilde Théry},
journal = {Journal of Extracellular Vesicles},
year = {2026},
month = nov,
doi = {10.1002/jev2.12242},
url = {https://hal.science/hal-03872914v2},
note = {CC BY-NC-ND 4.0},
}
RIS
TY - JOUR
TI - Homosalate boosts the release of tumour‐derived extracellular vesicles with protection against anchorage‐loss property
AU - Eleonora Grisard
AU - Nathalie Nevo
AU - Aurianne Lescure
AU - Sebastian Doll
AU - Maxime Corbé
AU - Mabel Jouve
AU - Gregory Lavieu
AU - Alain Joliot
AU - Elaine Del Nery
AU - Lorena Martin-Jaular
AU - Clotilde Théry
PY - 2026
DA - 2026/11/04
JO - Journal of Extracellular Vesicles
DO - 10.1002/jev2.12242
UR - https://hal.science/hal-03872914v2
AB - Eukaryotic cells, including cancer cells, secrete highly heterogeneous populations of extracellular vesicles (EVs). EVs could have different subcellular origin, composition and functional properties, but tools to distinguish between EV subtypes are scarce. Here, we tagged CD63- or CD9-positive EVs secreted by triple negative breast cancer cells with Nanoluciferase enzyme, to set-up a miniaturized method to quantify secretion of these two EV subtypes directly in the supernatant of cells. We performed a cell-based high-content screening to identify clinically-approved drugs able to affect EV secretion. One of the identified hits is Homosalate, an anti-inflammatory drug found in sunscreens which robustly increased EVs' release. Comparing EVs induced by Homosalate with those induced by Bafilomycin A1, we demonstrate that: (1) the two drugs act on EVs generated in distinct subcellular compartments, and (2) EVs released by Homosalate-, but not by Bafilomycin A1-treated cells enhance resistance to anchorage loss in another recipient epithelial tumour cell line. In conclusion, we identified a new drug modifying EV release and demonstrated that under influence of different drugs, triple negative breast cancer cells release EV subpopulations from different subcellular origins harbouring distinct functional properties.
SN - 2001-3078
ER -