ArticleOncotarget2016
Intracellular STING inactivation sensitizes breast cancer cells to genotoxic agents.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 51 papers, 1 of them a synthesis that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
51 citing papers in PubMed, 1 synthesis or guideline pooled it, 74 citations in OpenAlex.
- Destabilizing the genome as a therapeutic strategy to enhance response to immune checkpoint blockade: a systematic review of clinical trials evidence from solid and hematological tumors.Frontiers in pharmacology · 2023Pooled it
- Detection of nuclear STING in cultured human cells and in the normal and cancer tissues.iScience · 2026Article
- Mono-ADP-ribosylating PARP enzymes in cellular signaling and disease.Journal of cell science · 2025Review
- cGAS and STING in Host Myeloid Cells Are Essential for Effective Cyclophosphamide Treatment of Advanced Breast Cancer.Cancers · 2025Article
- PARP12-mediated ADP-ribosylation contributes to breast cancer cell fate by regulating AKT activation and DNA-damage response.Cellular and molecular life sciences : CMLS · 2025Article
- Unveiling Promising PARP12 Inhibitors through Virtual Screening for Cancer Therapy.Current pharmaceutical design · 2025Article
- Chronic interferon-stimulated gene transcription promotes oncogene-induced breast cancer.Genes & development · 2024Article
- Loss of the DNA repair protein, polynucleotide kinase/phosphatase, activates the type 1 interferon response independent of ionizing radiation.Nucleic acids research · 2024Article
- PARP enzymes and mono-ADP-ribosylation: advancing the connection from interferon-signalling to cancer biology.Expert reviews in molecular medicine · 2024Review
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- The tumor cell-intrinsic cGAS-STING pathway is associated with the high density of CD8Esophagus : official journal of the Japan Esophageal Society · 2024Article
- An inflamed tumor cell subpopulation promotes chemotherapy resistance in triple negative breast cancer.Scientific reports · 2024Article
- Harnessing the cGAS-STING pathway to potentiate radiation therapy: current approaches and future directions.Frontiers in pharmacology · 2024Review
- The Role of the Toll-like Receptor 2 and the cGAS-STING Pathways in Breast Cancer: Friends or Foes?International journal of molecular sciences · 2023Review
- Privileged Scaffolds for Potent and Specific Inhibitors of Mono-ADP-Ribosylating PARPs.Molecules (Basel, Switzerland) · 2023Review
- Long non‑coding RNAs as potential therapeutic targets in non‑small cell lung cancer (Review).International journal of molecular medicine · 2023Review
- cGAS-STING signalling in cancer: striking a balance with chromosomal instability.Biochemical Society transactions · 2023Review
- Protein Expression of immune checkpoints STING and MHCII in small cell lung cancer.Cancer immunology, immunotherapy : CII · 2023Article
- Epigenetic modulation of antitumor immunity and immunotherapy response in breast cancer: biological mechanisms and clinical implications.Frontiers in immunology · 2023Review
Corrections and comments
- Erratum issued
Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Activation of the IFN/STAT1 pathway is closely associated with drug response and recurrence of breast cancer treated by chemotherapy. The aim of the current study was to elucidate the molecular mechanisms involved upstream and downstream of this pathway in order to identify distinct entities that might be manipulated to improve treatment efficacy. Four breast cancer cell lines (T-47D, MCF7, MDA-MB-231 and HBCx-19 established from the eponymous PDX) were treated in vitro with mafosfamide, a DNA damage inducer. In two of these cell lines (MCF7 and HBCx-19), genotoxic treatment upregulated type I IFN expression leading to paracrine activation of IFN/STAT1 signaling pathway after 6-8 days. We show that STING, a well-characterized inducer of IFN in immune cells, is rapidly triggered in MCF7 cells under genotoxic stress and forms nuclear foci that co-localize with phosphorylated IRF-3 and γH2AX. STING silencing abrogated chemotherapy-induced type I IFN production and signaling and potentiated genotoxic treatment efficacy as it promoted cell death extent and delayed cell colony regrowth. Similar results were obtained after silencing PARP12, one selected gene of the IFN/STAT1 pathway fingerprint. In summary, this study provides the first demonstration of STING activation in breast cancer cells. Our data suggest that genotoxic-induced, STING-mediated type I IFN signaling is a cell-intrinsic mechanism of breast cancer cell survival and regrowth.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.