Inflammation-driven carcinogenesis is mediated through STING

Jeonghyun Ahn, Tianli Xia, Hiroyasu Konno, Keiko Konno, Phillip Ruiz and Glen N. Barber ()
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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

Nature Communications, 2014, vol. 5, issue 1, 1-9

Abstract: 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.

Date: 2014
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DOI: 10.1038/ncomms6166

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