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Inflammation-driven carcinogenesis is mediated through STING

Author

Listed:
  • Jeonghyun Ahn

    (University of Miami School of Medicine)

  • Tianli Xia

    (University of Miami School of Medicine)

  • Hiroyasu Konno

    (University of Miami School of Medicine)

  • Keiko Konno

    (University of Miami School of Medicine)

  • Phillip Ruiz

    (University of Miami School of Medicine)

  • Glen N. Barber

    (University of Miami School of Medicine)

Abstract

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.

Suggested Citation

  • Jeonghyun Ahn & Tianli Xia & Hiroyasu Konno & Keiko Konno & Phillip Ruiz & Glen N. Barber, 2014. "Inflammation-driven carcinogenesis is mediated through STING," Nature Communications, Nature, vol. 5(1), pages 1-9, December.
    • Handle: RePEc:nat:natcom:v:5:y:2014:i:1:d:10.1038_ncomms6166
    DOI: 10.1038/ncomms6166
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