The cGAS-STING pathway plays a crucial role in activating dendritic cells (DCs) and enhancing anticancer immunity. Type I Interferons (IFN-I) are essential for tumor therapy, but the specific mechanisms by which they activate DCs remain unclear. The cGAS-STING pathway, which is activated by aberrant DNA in the cytoplasm, produces IFN-I, which is vital for antiviral and anticancer immunity. STING can also enhance anticancer immunity by promoting autophagy, inflammation, and glycolysis in an IFN-I-independent manner. This review aims to summarize the novel mechanisms underlying the cGAS-STING-IFN-I signal activation in DC-mediated antigen presentation and its role in the cancer immune cycle. DCs are specialized antigen-presenting cells that play a pivotal role in initiating the tumor immune cycle by processing and presenting tumor antigens to T cells. The cGAS-STING pathway is essential for the activation and maturation of DCs, enhancing their antigen presentation capacity and promoting T cell activation. IFN-I exerts diverse effects on DCs, including upregulating surface molecules, inducing the expression of interferon-stimulated genes (ISGs), and facilitating cross-priming of CD8+ T cells. The cGAS-STING pathway also exhibits unique characteristics, such as inducing autophagy and promoting the NF-κB-mediated inflammatory response. Recent studies have revealed that STING can influence tumor dynamics through various mechanisms, including autophagy, endoplasmic reticulum stress, and cellular metabolism. STING agonists not only stimulate the production of IFN-I but also activate cellular stress and death pathways, leading to T cell apoptosis. The development of STING agonists presents broader potential in cancer therapy compared to IFN-I, with diverse formats such as protein drugs, small-molecule drugs, and gene therapy drugs. Clinical advancements in IFN-I drugs include the use of PEG-IFN to enhance stability and half-life, and the development of antibody-conjugated IFN-I for targeted therapy. STING agonists, such as DMXAA and ADU-S100/MIW815, have shown promise in preclinical studies but require further optimization for clinical efficacy. The cGAS-STING-IFN-I signaling axis is a master regulator in the cancer immunity cycle, influencing nearly all stages of tumor immune responses.The cGAS-STING pathway plays a crucial role in activating dendritic cells (DCs) and enhancing anticancer immunity. Type I Interferons (IFN-I) are essential for tumor therapy, but the specific mechanisms by which they activate DCs remain unclear. The cGAS-STING pathway, which is activated by aberrant DNA in the cytoplasm, produces IFN-I, which is vital for antiviral and anticancer immunity. STING can also enhance anticancer immunity by promoting autophagy, inflammation, and glycolysis in an IFN-I-independent manner. This review aims to summarize the novel mechanisms underlying the cGAS-STING-IFN-I signal activation in DC-mediated antigen presentation and its role in the cancer immune cycle. DCs are specialized antigen-presenting cells that play a pivotal role in initiating the tumor immune cycle by processing and presenting tumor antigens to T cells. The cGAS-STING pathway is essential for the activation and maturation of DCs, enhancing their antigen presentation capacity and promoting T cell activation. IFN-I exerts diverse effects on DCs, including upregulating surface molecules, inducing the expression of interferon-stimulated genes (ISGs), and facilitating cross-priming of CD8+ T cells. The cGAS-STING pathway also exhibits unique characteristics, such as inducing autophagy and promoting the NF-κB-mediated inflammatory response. Recent studies have revealed that STING can influence tumor dynamics through various mechanisms, including autophagy, endoplasmic reticulum stress, and cellular metabolism. STING agonists not only stimulate the production of IFN-I but also activate cellular stress and death pathways, leading to T cell apoptosis. The development of STING agonists presents broader potential in cancer therapy compared to IFN-I, with diverse formats such as protein drugs, small-molecule drugs, and gene therapy drugs. Clinical advancements in IFN-I drugs include the use of PEG-IFN to enhance stability and half-life, and the development of antibody-conjugated IFN-I for targeted therapy. STING agonists, such as DMXAA and ADU-S100/MIW815, have shown promise in preclinical studies but require further optimization for clinical efficacy. The cGAS-STING-IFN-I signaling axis is a master regulator in the cancer immunity cycle, influencing nearly all stages of tumor immune responses.