Fiche publication
Date publication
août 2026
Journal
Developmental cell
Auteurs
Membres identifiés du Cancéropôle Est :
Dr HERAULT Yann
,
Mme MESSADDEQ Nadia
Tous les auteurs :
Durik M, Karout M, Sampaio Gonçalves D, Knauer-Meyer T, Spiegelhalter C, Messaddeq N, Seehawer M, Stephan P, Bulavin DV, Herault Y, Zender L, Keyes WM
Lien Pubmed
Résumé
Cellular senescence is a state of stable arrest and secretion linked to aging and disease. Here, we identify that senescent cells dispose of large fragments through cell-to-cell adhesion, which we term "senescent-cell adhesion fragments" (SCAFs). Found in many senescent states, including human and mouse cells, and mouse tissues, SCAFs lack nuclear material but contain organelles, including damaged mitochondria. Disrupting adherens junctions decreases SCAF formation but induces senescent-cell death, due to an inability to shed damaged mitochondria. Live imaging and proteomics show that SCAFs ultimately rupture, releasing a complex proteome, including damage-associated molecular patterns (DAMPs) and proteins linked to neurodegenerative disease. Functionally, SCAFs activate wound-healing and cancer-related programs, promoting migration and invasion. Immunostaining also reveals amyloid-like material in senescent cells that can be externalized through fragmentation. Altogether, these findings identify a feature that facilitates senescent cell survival but also externally deposits damaged intracellular contents, with implications for cancer and neurodegeneration.
Mots clés
DAMPs, aging, amyloid, cancer, cell-cell adhesion, debris, mitochondria, senescence
Référence
Dev Cell. 2026 08 28;:
