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STING-dependent paracriny shapes apoptotic priming of breast tumors in response to anti-mitotic treatment.

Abstract：

:A fascinating but uncharacterized action of antimitotic chemotherapy is to collectively prime cancer cells to apoptotic mitochondrial outer membrane permeabilization (MOMP), while impacting only on cycling cell subsets. Here, we show that a proapoptotic secretory phenotype is induced by activation of cGAS/STING in cancer cells that are hit by antimitotic treatment, accumulate micronuclei and maintain mitochondrial integrity despite intrinsic apoptotic pressure. Organotypic cultures of primary human breast tumors and patient-derived xenografts sensitive to paclitaxel exhibit gene expression signatures typical of type I IFN and TNFα exposure. These cytokines induced by cGAS/STING activation trigger NOXA expression in neighboring cells and render them acutely sensitive to BCL-xL inhibition. cGAS/STING-dependent apoptotic effects are required for paclitaxel response in vivo, and they are amplified by sequential, but not synchronous, administration of BH3 mimetics. Thus anti-mitotic agents propagate apoptotic priming across heterogeneously sensitive cancer cells through cytosolic DNA sensing pathway-dependent extracellular signals, exploitable by delayed MOMP targeting.

journal_name

Nat Commun

journal_title

Nature communications

authors

Lohard S,Bourgeois N,Maillet L,Gautier F,Fétiveau A,Lasla H,Nguyen F,Vuillier C,Dumont A,Moreau-Aubry A,Frapin M,David L,Loussouarn D,Kerdraon O,Campone M,Jézéquel P,Juin PP,Barillé-Nion S

doi

10.1038/s41467-019-13689-y

subject

Has Abstract

pub_date

2020-01-14 00:00:00

pages

259

issue

1

issn

2041-1723

pii

10.1038/s41467-019-13689-y

journal_volume

11

pub_type

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