Skip to main content
. 2020 Jun 16;9(1):1777624. doi: 10.1080/2162402X.2020.1777624

Figure 1.

Figure 1.

Overview of STING signaling in cancer cells. Accumulation of double-stranded DNA (dsDNA) in the cytosol of cancer cells responding to some chemotherapeutics or radiation therapy boosts the enzymatic functions of cyclic GMP-AMP synthase (CGAS), resulting in the cyclic GMP-AMP (cGAMP)-dependent oligomerization and activation of stimulator of interferon response cGAMP interactor 1 (STING1, best known as STING) at the endoplasmic reticulum (ER). Activated STING promotes a TANK binding kinase 1 (TAK1)-dependent signal transduction cascade that initiates interferon regulatory factor 3 (IRF3)- and NF-κB-dependent transcription, potentially culminating with the secretion of numerous cytokines including type I interferon (IFN), interleukin 6 (IL-6) and tumor necrosis factor (TNF). CDN, cyclic dinucleotide; IκBα (official name: NFKBIA), NFKB inhibitor alpha; IKKα (official name: CHUK), component of inhibitor of nuclear factor-kappa B kinase complex; IKKβ (official name: IKBKB), inhibitor of nuclear factor-kappa B kinase subunit beta; PARP, poly(ADP-ribose) polymerase.