ArticleCurrent cancer drug targets2026
GPX4 Inhibition Enhances the Antitumor Effect of PARP Inhibitor on Homologous Recombination Proficient Ovarian Cancer Cells.
Article in Current cancer drug targets, 2026. 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.
- Advances in ferroptosis research in ovarian cancer: molecular mechanisms and therapeutic perspectives.American journal of cancer research · 2026Review
- Omics integration identified CRIP2 as a key mediator of olaparib resistance in prostate cancer.Translational andrology and urology · 2025Article
- Research progress on ferroptosis and PARP inhibitors in ovarian cancer: action mechanisms and resistance mechanisms.Frontiers in pharmacology · 2025Review
- Research on the function of GPX4 in tumor-targeted treatment based on its molecular structure and features.Frontiers in oncology · 2025Review
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11 authors.
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Abstract
backgroundPoly (ADP-ribose) polymerase inhibitors (PARPi) are now widely used in BRCA1/2 mutation or homologous recombination (HR) deficiency ovarian cancer but have limited efficacy in HR-proficient patients. GPX4 is a key regulator of ferroptosis and has been proven to be associated with multiple drug sensitivities. As a molecule that regulates the sensitivity of multiple drugs, the relationship between GPX4 and the efficacy of PARPi in HR-proficient ovarian cancer has not been elucidated.
methodsIn this study, siRNA transfection was used to regulate the expression of GPX4. The effect of GPX4 inhibition on HR-proficient ovarian cancer was determined by CCK-8 assay and flow cytometry. Immunofluorescence and comet assay were used to reflect DNA damage. ROS production was measured using DCFH-DA and flow cytometry. The combination index of PARP inhibitors and RSL3 was calculated using CompuSyn software based on Chou- Talalay methodology.
resultsGPX4 inhibition confers HR-proficient ovarian cancer cells sensitive to PARPi due to ROS generation and oxidative stress caused DNA double-strand breakage. The combination of olaparib and niraparib with GPX4 inhibitor RSL3 also showed a synergistic effect.
conclusionCombining GPX4 inhibition with PARP inhibitors resulted in a notable increase in DNA damage, ultimately causing the death of cancer cells with proficient HR pathways. Our findings may provide new therapeutic options for HR-proficient patients to benefit from PARP inhibitors and improve outcomes.
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