期刊
CELL CYCLE
卷 18, 期 16, 页码 1830-1848出版社
TAYLOR & FRANCIS INC
DOI: 10.1080/15384101.2019.1638192
关键词
Genomic instability; cytoplasmic DNA; cGAS; STING; interferon response; inflammatory signaling
类别
资金
- European Research Council [682421]
- Dutch Cancer Society/Alpe d'HuZes [EMCR2014-7048]
- European Research Council (ERC) [682421] Funding Source: European Research Council (ERC)
Recent studies have shown that genomic instability in tumor cells leads to activation of inflammatory signaling through the cGAS/STING pathway. In this review, we describe multiple ways by which genomic instability leads to cGAS/STING-mediated inflammatory signaling, as well as the consequences for tumor development and the tumor microenvironment. Also, we elaborate on how tumor cells have apparently evolved to escape the immune surveillance mechanisms that are triggered by cGAS/STING signaling. Finally, we describe how cGAS/STING-mediated inflammatory signaling can be therapeutically targeted to improve therapy responses.
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