Extracellular vesicles released by senescent tumor cells are both necessary and sufficient to transmit senescence to neighboring cells, independent of soluble secretory factors. Blocking vesicle biogenesis pharmacologically or by silencing RAB27A prevented this spread without altering the senescent state of the producer cells. Vesicular transport, rather than the broader secretory phenotype, emerges as the decisive channel through which senescence propagates through tissue.
Key Points
- Senescent tumor cell vesicles alone induce senescence in recipient cells
- Blocking vesicle release halts spread without changing soluble secretions
- Senescent vesicle cargo enriched for wound healing and hemostasis proteins
Longevity Analysis
Senescent cell burden accumulates with age and contributes to chronic inflammation, impaired tissue repair, and declining regenerative capacity. Identifying vesicles as the transmissible unit of senescence narrows the target from a diffuse inflammatory secretome to a specific transport pathway, one that could be interrupted without disturbing the producer cells themselves. For therapy-induced senescence following cancer treatment, this offers a route to contain the damage signal before it propagates through surrounding tissue and taxes immune surveillance.
Original published by Wiley Aging Cell, by Valentin Estevez‐Souto, Alex Miralles‐Dominguez, Pablo Pedrosa, Patricia Lado‐Fernandez, Miguel A. Prados, Alejandro Failde‐Fiestras, Raquel Paredes‐Paredes, Jorge Ruz‐Ortega, Maria J. Alonso, Martina Migliavacca, Ester Polo, Rebeca Alvarez‐Velez, Enrique Vazquez de Luis, Ana Dopazo, Gabriela N. Condezo, Carmen San Martin, Miguel Gonzalez‐Barcia, Ramón Lobato‐Busto, Pilar Ximénez‐Embún, Javier Muñoz, Manuel Collado, Sabela Da Silva‐Alvarez .