cGAS-STING signaling in melanoma: regulation and therapeutic targeting
摘要
Melanocytes are the source of the skin cancer known as melanoma. It usually affects the viscera, mucous membranes, and skin. Even so, melanoma only makes for 7% of all skin cancer occurrences. By triggering the generation of type I interferons (IFN-I) and inflammatory cytokines upon identifying microbial DNA, the cyclic GMP-AMP synthase (cGAS)–stimulator of interferon genes (STING) pathway promotes anti-microbial innate immunity. A growing body of research indicates that antitumor immunity depends on the cGAS-STING axis being activated. The cGAS-STING-regulated downstream cytokines, particularly IFN-I, act as linkages between adaptive and innate immunity. As a result, an increasing amount of research has concentrated on the synthesis and screening of agonists of the STING pathway. As a result, an increasing amount of research has concentrated on the synthesis and screening of agonists of the STING pathway. The many implications of the cGAS-STING pathway in the pathophysiology and therapy of melanoma are thoroughly examined in this study. Our research highlights the significance of the cGAS-STING pathway in melanoma and identifies it as a key target for boosting immunity against tumors.