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Updated: Feb 5, 2026

Using RNA-sequencing to Detect Novel Splice Variants Related to Drug Resistance in In Vitro Cancer Models
Published on: December 9, 2016
Pharmacological activation of cGAS-STING pathway to reverse cancer drug resistance
Yumin Wang1, Yan Wang2, Qingzhu Gao3
1Department of Respiratory and Critical Care Medicine, Aerospace Center Hospital, Peking University Aerospace School of Clinical Medicine, Beijing 100049, China.
Abstract:
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.
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