Therapeutic resistance remains a major challenge in cancer management. The cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) pathway senses cytosolic DNA and triggers innate immune responses. Cancer cells frequently acquire drug resistance by inhibiting cGAS-STING signaling, leading to growing interest in small-molecule agonists that reactivate this pathway to counter resistance. In this review, we summarize recent molecular and cellular findings explaining how cancer cells suppress cGAS-STING through epigenetic regulation, post-translational modifications (PTMs), and altered metabolic pathways. We also evaluate recent studies on cGAS-STING agonists aimed at restoring sensitivity to chemotherapy, immunotherapy, and targeted cancer therapies to inform new strategies to pharmacologically reactivate cGAS-STING signaling pathway to reverse existing therapeutic barriers.
Building similarity graph...
Analyzing shared references across papers
Loading...
Yumin Wang
Yan Wang
Qingzhu Gao
Pharmacology & Therapeutics
Johns Hopkins University
Peking University
Central South University
Building similarity graph...
Analyzing shared references across papers
Loading...
Wang et al. (Sun,) studied this question.
www.synapsesocial.com/papers/69a76555badf0bb9e87d8bcd — DOI: https://doi.org/10.1016/j.pharmthera.2026.108991