Decrypting the Crosstalk Mechanisms Between cGAS-STING and TBK1 Signaling Pathways in Cancer Immunotherapy: A Comprehensive Review
DOI:
https://doi.org/10.62382/jcbt.v2i1.42Keywords:
cGAS-STING, TBK1, Tumor Microenvironment, Immunity, Cancer ImmunotherapyAbstract
In the tumor microenvironment, the cytosolic DNA sensing, cyclic GMP-AMP synthase- stimulator of interferon genes (cGAS-STING) pathway is a crucial regulator of immune response. The cGAS of innate immunity recognizes cytoplasmic DNA by catalyzing cyclic GMP-AMP (cGAMP), which subsequently activates the STING pathway. STING activation leads to the phosphorylation of TANK-binding kinase 1 (TBK1) and recruitment of key transcription factor IRF3, notably to initiate the production of pro-inflammatory cytokines and Type I IFNs. This cascade enhances antigen presentation and primes cytotoxic T-cells, leading to the induction of anti-tumor immune response. Specific crosstalk mechanisms, such as TBK1-mediated negative feedback to limit excessive STING activation or its cooperation with NF-κB to balance immune responses, play pivotal roles in shaping tumor immunity. Harnessing this axis in cancer immunotherapy has emerged as a promising strategy, offering synergy with immune checkpoint blockade and CAR T-cells therapy. Fine-tuning activation of this pathway is crucial for balanced immune responses, making cGAS-STING/TBK1 signal transduction a major target for novel cancer therapies. This review elucidates the intricate crosstalk mechanisms of cGAS-STING and TBK1 signal transduction within tumor microenvironment. These may shed insight on cancer therapy options and their pivotal roles in modulating tumor immunity.
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