Correction: Intracellular STING inactivation sensitizes breast cancer cells to genotoxic agents

Gaston, Julie; Cheradame, Laura; Yvonnet, Vanessa; Déas, Olivier; Poupon, Marie‐France; Judde, Jean-Gabriel; Cairo, Stefano; Goffin, Vincent

doi:10.18632/oncotarget.27042

Cited by 3 publications

(2 citation statements)

References 3 publications

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“…more efficient transfection efficiency). To avoid specificity issues encountered in immunocytofluorescence experiments using commercial anti-STING antibodies (Gaston et al 2019), we generated Flag and/or hemagglutinin (HA)-tagged STING constructs. The latter displayed similar fractionation profile as endogenous STING when ectopically-expressed in MCF7 cells (Fig.…”

Section: Resultsmentioning

confidence: 99%

STING Promotes Breast Cancer Cell Survival by an Inflammatory-Independent Nuclear Pathway Enhancing the DNA Damage Response

Cheradame

Guerrera

Gaston

et al. 2020

Preprint

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STING (Stimulator of Interferon Genes) is a well-known endoplasmic reticulum-anchored adaptor of the innate immunity that triggers the expression of inflammatory cytokines in response to pathogen infection. In cancer cells, this pro-inflammatory pathway can be activated by genomic DNA damage potentiating antitumor immune responses. Here we report that STING promotes cancer cell survival and resistance to genotoxic treatment in a cell-autonomous manner. Mechanistically, we show that STING partly localizes at the inner nuclear membrane in various breast cancer cell lines and clinical tumor samples, and interacts with several proteins of the DNA damage response (DDR). STING overexpression enhances the amount of chromatin-bound DNA-dependent Protein Kinase (DNA-PK) complex, while STING silencing impairs DDR foci formation and DNA repair efficacy. Importantly, this function of STING is independent of its canonical pro-inflammatory pathway. This study highlights a previously unappreciated cell-autonomous tumor-promoting mechanism of STING that opposes its well-documented role in tumor immunosurveillance.

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Section: Resultsmentioning

confidence: 99%

STING Promotes Breast Cancer Cell Survival by an Inflammatory-Independent Nuclear Pathway Enhancing the DNA Damage Response

Cheradame

Guerrera

Gaston

et al. 2020

Preprint

Self Cite

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“…For example, several studies have shown that the expression of a subset of interferon-stimulated genes (ISGs), known as the IFN-related DNA damage resistance signature (IRDS), which is associated with resistance to DNA-damaging chemo- and radiotherapies [ 39–41 ] is sustained by cGAS–STING-driven IFN activation following prolonged DNA damage [ 42–44 ]. Although the full extent of mechanisms underlying the protective nature of certain chronic IFN responses remains unknown, two studies linked persistent STING activity with the IFN-driven expression of several PARP -family genes, including PARP9 and PARP12, posited to promote tumour cell resistance to genotoxic stresses [ 43 , 45 ] by enhancing DNA damage repair responses [ 46 ].…”

Section: Cell-intrinsic Functions Of Cgas–sting In Cin: Genome Stabil...mentioning

confidence: 99%

cGAS–STING signalling in cancer: striking a balance with chromosomal instability

Beernaert

Parkes

2023

Biochemical Society Transactions

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Chromosomal instability (CIN) is a hallmark of cancer that drives tumour evolution. It is now recognised that CIN in cancer leads to the constitutive production of misplaced DNA in the form of micronuclei and chromatin bridges. These structures are detected by the nucleic acid sensor cGAS, leading to the production of the second messenger 2′3′-cGAMP and activation of the critical hub of innate immune signalling STING. Activation of this immune pathway should instigate the influx and activation of immune cells, resulting in the eradication of cancer cells. That this does not universally occur in the context of CIN remains an unanswered paradox in cancer. Instead, CIN-high cancers are notably adept at immune evasion and are highly metastatic with typically poor outcomes. In this review, we discuss the diverse facets of the cGAS–STING signalling pathway, including emerging roles in homeostatic processes and their intersection with genome stability regulation, its role as a driver of chronic pro-tumour inflammation, and crosstalk with the tumour microenvironment, which may collectively underlie its apparent maintenance in cancers. A better understanding of the mechanisms whereby this immune surveillance pathway is commandeered by chromosomally unstable cancers is critical to the identification of new vulnerabilities for therapeutic exploitation.

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STING protects breast cancer cells from intrinsic and genotoxic-induced DNA instability via a non-canonical, cell-autonomous pathway

et al. 2021

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Correction: Intracellular STING inactivation sensitizes breast cancer cells to genotoxic agents

Cited by 3 publications

References 3 publications

STING Promotes Breast Cancer Cell Survival by an Inflammatory-Independent Nuclear Pathway Enhancing the DNA Damage Response

STING Promotes Breast Cancer Cell Survival by an Inflammatory-Independent Nuclear Pathway Enhancing the DNA Damage Response

cGAS–STING signalling in cancer: striking a balance with chromosomal instability

STING protects breast cancer cells from intrinsic and genotoxic-induced DNA instability via a non-canonical, cell-autonomous pathway

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