Abstract
Cytosolic DNA is prevalent in cells constituting the tumor microenvironment (TME) and can activate the cyclic guanosine monophosphate–adenosine monophosphate synthase (cGAS)–stimulator of interferon genes (STING) innate immune pathway. The initiation, transmission, and execution of the cGAS–STING pathway can take place among different cell types within the TME and thus cGAS–STING may play opposing roles in driving tumor progression in addition to its tumor cell-intrinsic role. Herein, we review recent advances in the cGAS–STING field with a focus on its crosstalk with other signaling pathways in the TME. Future efforts to depict a more detailed picture of the roles of cGAS–STING signaling in the TME will help design a better cancer treatment regime by targeting the cGAS–STING pathway more precisely.
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