The DOI matches its Crossref record; 24 of the 24 references it cites were found in a registry or an index.
Inflammation-driven carcinogenesis is mediated through STING
Open accessAbstract
Chronic stimulation of innate immune pathways by microbial agents or damaged tissue is known to promote inflammation-driven tumorigenesis by mechanisms that are not well understood. Here we demonstrate that mutagenic 7,12-dimethylbenz(a)anthracene (DMBA), cisplatin and etoposide induce nuclear DNA leakage into the cytosol that intrinsically activates stimulator of interferon genes (STING)-dependent cytokine production. Inflammatory cytokine levels are subsequently augmented in a STING-dependent extrinsic manner by infiltrating phagocytes purging dying cells. Consequently, STING−/− mice, or wild-type mice adoptively transferred with STING−/− bone marrow, are almost completely resistant to DMBA-induced skin carcinogenesis compared with their wild-type counterparts. Our data establish a role for STING in the control of cancer, shed significant insight into the causes of inflammation-driven carcinogenesis and may provide a basis for therapeutic strategies to help prevent malignant disease. Chronic inflammation is known to promote tumorigenesis, but the mechanisms underlying this are incompletely understood. Here, the authors show that several carcinogens induce DNA leakage into the cytoplasm, which activates STING-dependent cytokine production and inflammation-driven tumorigenesis.
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Cites
Immunity, Inflammation, and Cancer
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Cyclic GMP-AMP Synthase Is a Cytosolic DNA Sensor That Activates the Type I Interferon Pathway
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STING is an endoplasmic reticulum adaptor that facilitates innate immune signalling
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Self-citationSTING regulates intracellular DNA-mediated, type I interferon-dependent innate immunity
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Self-citationCancer risk from occupational and environmental exposure to polycyclic aromatic hydrocarbons
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Langerhans cells renew in the skin throughout life under steady-state conditions
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Autoimmunity and the Clearance of Dead Cells
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Mice deficient in tumor necrosis factor-α are resistant to skin carcinogenesis
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Cited by
The cGAS–STING pathway as a therapeutic target in inflammatory diseases
Decout, A., Katz, J. D., Venkatraman, S., & Ablasser, A. (2021) · Nature Reviews Immunology · doi:10.1038/s41577-021-00524-z · Cited by 2,309
Molecular mechanisms and cellular functions of cGAS–STING signalling
Hopfner, K.-P., & Hornung, V. (2020) · Nature Reviews Molecular Cell Biology · doi:10.1038/s41580-020-0244-x · Cited by 2,052
DNA exonuclease Trex1 regulates radiotherapy-induced tumour immunogenicity
Vanpouille-Box, C., Alard, A., Aryankalayil, M. J., Sarfraz, Y., Diamond, J. M., Schneider, R. J., Inghirami, G., Coleman, C. N., Formenti, S. C., & Demaria, S. (2017) · Nature Communications · doi:10.1038/ncomms15618 · Cited by 1,834
cGAS surveillance of micronuclei links genome instability to innate immunity
Mackenzie, K. J., Carroll, P., Martin, C.-A., Murina, O., Fluteau, A., Simpson, D. J., Olova, N., Sutcliffe, H., Rainger, J. K., Leitch, A., et al. (2017) · Nature · doi:10.1038/nature23449 · Cited by 1,752
DAMP-sensing receptors in sterile inflammation and inflammatory diseases
Gong, T., Liu, L., Jiang, W., & Zhou, R. (2020) · Nature Reviews Immunology · doi:10.1038/s41577-019-0215-7 · Cited by 1,672
Metadata
- Authors
- Ahn, J., Xia, T., Konno, H., Konno, K., Ruiz, P., & Barber, G. N.
- Venue
- Nature Communications
- Published
- 2014-10-10
- Volume
- 5
- Issue
- 1
- Pages
- 5166-5166
- ISSN
- 2041-1723 (ISSN-L)
- OpenAlex
- W2046640968
- Cited by
- 447
- References
- 24
- FWCI
- 8.69
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Ahn, J., Xia, T., Konno, H., Konno, K., Ruiz, P., & Barber, G. N. (2014). Inflammation-driven carcinogenesis is mediated through STING. Nature Communications. https://doi.org/10.1038/ncomms6166
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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