Deregulation of STING Signaling in Colorectal Carcinoma Constrains DNA Damage Responses and Correlates With Tumorigenesis

Cell Rep. 2016 Jan 12;14(2):282-97. doi: 10.1016/j.celrep.2015.12.029. Epub 2015 Dec 31.


Stimulator of interferon genes (STING) has been shown to be critical for controlling antiviral responses as well as anti-tumor adaptive immunity, but little is known regarding its regulation in human tumors. Here, we report that STING signaling is recurrently suppressed in a wide variety of cancers, including colorectal carcinoma. Loss of STING signaling impeded DNA damage responses accountable for generating key cytokines that facilitate tissue repair and anti-tumor T cell priming, such as type I interferons (IFNs). Correspondingly, defective STING function was also highly predictive of effectual DNA-virus-mediated oncolytic activity. Thus, impaired STING responses may enable damaged cells to evade host immunosurveillance processes, although they provide a critical prognostic measurement that could help predict the outcome of effective oncoviral therapy.

MeSH terms

  • Animals
  • Carcinogenesis / genetics*
  • Colorectal Neoplasms / genetics*
  • DNA Damage / genetics*
  • Humans
  • Mice
  • Signal Transduction
  • Transfection