ArticleInternational journal of clinical and experimental pathology2024
Activation of cGAS confers PARP inhibitor resistance in ovarian cancer via the TBK1-IRF3 axis.
Article in International journal of clinical and experimental pathology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Expanding Synthetic Lethality in DNA Damage Response-Defective Cancers Through Stress Phenotype-Guided Kinase Targeting.International journal of molecular sciences · 2026Review
- Clinical application of PARP inhibitors and emerging strategies to overcome resistance: a pan-cancer perspective.Biomarker research · 2026Review
- Comparative Protective Effects of ATP and TPP Against Olaparib-Induced Ovarian Injury in Rats: Insights from Biochemical Parameters, Histopathology, and IRE1α, Cleaved Caspase-3, LC3B, and NF-κB p65 Double Immunofluorescence.Drug design, development and therapy · 2026Article
- PARylation-centric crosstalk: orchestrating immune evasion and multidrug resistance in ovarian cancer.Frontiers in immunology · 2026Review
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Authors and funding
12 authors.
Funding
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Abstract
objectivesOvarian cancer is a gynecologic tumor with the highest mortality rate worldwide. Nonetheless, chemoresistance remains a significant obstacle in treating ovarian cancer. PARP inhibitors (PARPis) are effective drugs approved for maintenance therapy in ovarian cancer. However, the development of natural or acquired resistance to PARPis poses a major challenge for ovarian cancer treatment.
methodsPublic database analysis of cGAS expression in relation to PARPi resistance. cCK-8 assay was used to determine cell survival. qPCR assay with Western Blot was implemented to determine gene expression and protein activation status.
resultsAnalysis of public databases revealed significantly higher cGAS expression in Olaparib-resistant cells and in recurrent ovarian tumors. Furthermore, high cGAS expression significantly promoted Olaparib tolerance in ovarian cancer cells. Our findings demonstrate that Olaparib treatment induces activation of the TBK1-IRF3 signaling axis downstream of cGAS, leading to the production of type I interferon. This, in turn, activates NF-κB and IL-6-STAT3 signaling, contributing to inflammation and PARPi resistance. Consequently, targeting cGAS effectively counteracts Olaparib resistance and enhances its efficacy in suppressing cancer cell growth, ultimately leading to cell death.
conclusionsOur study highlights the crucial function of cGAS signaling in mediating PARPi resistance in ovarian cancer cells. These findings provide valuable novel therapeutic strategies targeting cGAS to improve the efficacy of PARPi-based treatments for ovarian cancer.
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