Research Progress of cGAS STING Pathway in Tumor Therapy

The cGAS-STING pathway's activation and regulatory mechanisms, as well as its possible involvement in carcinogenesis and cancer treatment, are explored in this article. As a crucial pattern recognition receptor, cGAS may recognize aberrant cytosolic double-stranded DNA, catalyze the synthesis of cGAMP, and activate the STING protein, which is located in the endoplasmic reticulum. This activation causes type I interferons to be secreted, transcription factors such IRF3 to be inducted, and inflammatory reactions that impact cell division and death. Because this route is continuously activated in the tumor microenvironment, it can promote tumor cell proliferation and immune surveillance evasion while also having anti-tumor actions and the potential to cause chronic inflammation. Additionally, the cGAS-STING pathway can produce a number of pro-inflammatory molecules that help immune cells destroy malignancies. Small chemical agonists that target the cGAS-STING pathway are currently being developed with encouraging results, and combined therapeutic approaches have showed promise. Future research is expected to further expand the application of cGAS-STING pathway activators in more types of tumors and in combination with other therapeutic approaches, bringing new hope for cancer patients. At the same time, we must be vigilant about the connection between abnormal activation of the cGAS-STING pathway and autoimmune diseases to ensure the safety and efficacy of treatments.