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Review

Immune Regulation of the cGAS-STING Signaling Pathway in the Tumor Microenvironment and Its Clinical Application

ORCID Icon, , , &
Pages 1501-1516 | Published online: 01 Mar 2021

Figures & data

Figure 1 The cGAS-STING signaling pathway. Exogenous and endogenous DNA activate cGAS to generate second messenger 2ʹ,3ʹ-cGAMP. After 2ʹ,3ʹ-cGAMP binds to the downstream receptor protein STING, STING transfers to golgi body and polymerization occurs, and then, TBK1, IRF3 and NF-κB were recruited. This promotes the phosphorylation of IRF3 and NF-κB and facilitates their entry into the nucleus, finally, the transcription of genes associated with inflammatory factors is activated.

Figure 1 The cGAS-STING signaling pathway. Exogenous and endogenous DNA activate cGAS to generate second messenger 2ʹ,3ʹ-cGAMP. After 2ʹ,3ʹ-cGAMP binds to the downstream receptor protein STING, STING transfers to golgi body and polymerization occurs, and then, TBK1, IRF3 and NF-κB were recruited. This promotes the phosphorylation of IRF3 and NF-κB and facilitates their entry into the nucleus, finally, the transcription of genes associated with inflammatory factors is activated.

Table 1 Clinical Trials of STING Agonists