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Cutting edge: STING mediates protection against colorectal tumorigenesis by governing the magnitude of intestinal inflammation

(2014) JOURNAL OF IMMUNOLOGY. 193(10). p.4779-4782
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Abstract
Stimulator of IFN genes (STING) is a cytoplasmic innate immune sensor for cyclic dinucleotides that also serves a dual role as an adaptor molecule for a number of intracellular DNA receptors. Although STING has important functions in the host defense against pathogens and autoimmune diseases, its physiological role in cancer is unknown. In this study, we show that STING-deficient mice are highly susceptible to colitis-associated colorectal cancer. Colons of STING-deficient mice exhibit significant intestinal damage and overt proliferation during early stages of tumorigenesis. Moreover, STING-deficient mice fail to restrict activation of the NF-kappa B- and STAT3-signaling pathways, which leads to increased levels of the proinflammatory cytokines IL-6 and KC. Therefore, our results identified an unexpected and important role for STING in mediating protection against colorectal tumorigenesis.
Keywords
INNATE IMMUNE SENSOR, INTRACELLULAR DNA, NLRP3 INFLAMMASOME, NUCLEIC-ACIDS, BACTERIAL RNA, TUMOR-CELLS, CANCER, STAT3, SURVIVAL, ACTIVATION

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Citation

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Chicago
Zhu, Qifan, Si Ming Man, Prajwal Gurung, Zhiping Liu, Peter Vogel, Mohamed Lamkanfi, and Thirumala-Devi Kanneganti. 2014. “Cutting Edge: STING Mediates Protection Against Colorectal Tumorigenesis by Governing the Magnitude of Intestinal Inflammation.” Journal of Immunology 193 (10): 4779–4782.
APA
Zhu, Qifan, Man, S. M., Gurung, P., Liu, Z., Vogel, P., Lamkanfi, M., & Kanneganti, T.-D. (2014). Cutting edge: STING mediates protection against colorectal tumorigenesis by governing the magnitude of intestinal inflammation. JOURNAL OF IMMUNOLOGY, 193(10), 4779–4782.
Vancouver
1.
Zhu Q, Man SM, Gurung P, Liu Z, Vogel P, Lamkanfi M, et al. Cutting edge: STING mediates protection against colorectal tumorigenesis by governing the magnitude of intestinal inflammation. JOURNAL OF IMMUNOLOGY. 2014;193(10):4779–82.
MLA
Zhu, Qifan, Si Ming Man, Prajwal Gurung, et al. “Cutting Edge: STING Mediates Protection Against Colorectal Tumorigenesis by Governing the Magnitude of Intestinal Inflammation.” JOURNAL OF IMMUNOLOGY 193.10 (2014): 4779–4782. Print.
@article{5809480,
  abstract     = {Stimulator of IFN genes (STING) is a cytoplasmic innate immune sensor for cyclic dinucleotides that also serves a dual role as an adaptor molecule for a number of intracellular DNA receptors. Although STING has important functions in the host defense against pathogens and autoimmune diseases, its physiological role in cancer is unknown. In this study, we show that STING-deficient mice are highly susceptible to colitis-associated colorectal cancer. Colons of STING-deficient mice exhibit significant intestinal damage and overt proliferation during early stages of tumorigenesis. Moreover, STING-deficient mice fail to restrict activation of the NF-kappa B- and STAT3-signaling pathways, which leads to increased levels of the proinflammatory cytokines IL-6 and KC. Therefore, our results identified an unexpected and important role for STING in mediating protection against colorectal tumorigenesis.},
  author       = {Zhu, Qifan and Man, Si Ming and Gurung, Prajwal and Liu, Zhiping and Vogel, Peter and Lamkanfi, Mohamed and Kanneganti, Thirumala-Devi},
  issn         = {0022-1767},
  journal      = {JOURNAL OF IMMUNOLOGY},
  keywords     = {INNATE IMMUNE SENSOR,INTRACELLULAR DNA,NLRP3 INFLAMMASOME,NUCLEIC-ACIDS,BACTERIAL RNA,TUMOR-CELLS,CANCER,STAT3,SURVIVAL,ACTIVATION},
  language     = {eng},
  number       = {10},
  pages        = {4779--4782},
  title        = {Cutting edge: STING mediates protection against colorectal tumorigenesis by governing the magnitude of intestinal inflammation},
  url          = {http://dx.doi.org/10.4049/jimmunol.1402051},
  volume       = {193},
  year         = {2014},
}

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