Mitotic stress-induced secretome primes cancer cells to apoptosis and maximizes paclitaxel response in breast tumors when combined with BCL-xL-targeting BH3 mimetics.

Autor: Lohard S; Université de Nantes, Nantes, France., Juin PP; Université de Nantes, Nantes, France.; INSERM, CRCINA, Nantes, France.; SIRIC ILIAD, Nantes, Angers, France.; ICO René Gauducheau, Saint Herblain, France., Barillé-Nion S; Université de Nantes, Nantes, France.; INSERM, CRCINA, Nantes, France.; SIRIC ILIAD, Nantes, Angers, France.
Jazyk: angličtina
Zdroj: Molecular & cellular oncology [Mol Cell Oncol] 2020 Mar 19; Vol. 7 (3), pp. 1735912. Date of Electronic Publication: 2020 Mar 19 (Print Publication: 2020).
DOI: 10.1080/23723556.2020.1735912
Abstrakt: We recently identified a previously unappreciated ability of antimitotics to propagate apoptotic priming across cancer cell populations. The underlying paracrine cytotoxic signal, fueled by undead cells activating the cGAS/STING pathway, is required for in vivo antitumor response and it can be further exploited by delayed, but not synchronous, BCL-xL inhibition.
(© 2020 Taylor & Francis Group, LLC.)
Databáze: MEDLINE
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