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

Tianli Xia, Hiroyasu Konno, Jeonghyun Ahn, Glen N. Barber

Research output: Contribution to journalArticlepeer-review

168 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)282-297
Number of pages16
JournalCell Reports
Volume14
Issue number2
DOIs
StatePublished - Jan 12 2016

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

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