ArticleNAR cancer2025
Synergistic enhancement of PARP inhibition via small molecule UNI66-mediated suppression of BRD4-dependent transcription of
Article in NAR cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Interplay Between Poly(ADP-ribosyl)ation and Specific Inner Cellular Events That Suggest Combination Strategies for Overcoming PARP Inhibitor Resistance.Pharmaceutics · 2026Review
- Targeting DNA repair mechanisms in cancer therapy: the role of small molecule DNA repair inhibitors.NAR cancer · 2025Review
- Reprogramming oncogenic mitochondria in pancreatic adenocarcinoma through BRD4 inhibition leads to programmed cell death.The Journal of pharmacology and experimental therapeutics · 2025Article
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Authors and funding
11 authors.
Funding
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Abstract
Targeted therapy leveraging synthetic lethality in homologous recombination (HR)-defective tumors, particularly in BRCA-mutated tumors through poly(ADP-ribose) polymerase (PARP)-dependent repair inhibition, has shown success. However, the challenge lies in the ability of the tumors to reactivate HR via diverse mechanisms, leading to resistance against PARP-dependent repair inhibition. Addressing this issue, the down-regulation of HR activity has been explored as a potential strategy to overcome PARP inhibitor-resistant tumors. Yet, the intricate modulation of HR gene expression in mammalian cells is still not fully understood. In this study, we used a small molecule, UNI66, identified from high-throughput screening, to investigate regulatory mechanisms of HR. UNI66 was observed to induce synthetic lethality in PARP1-deficient cells and enhanced the sensitivity of multiple cancer cells to PARP inhibitors, suggesting a role in HR down-regulation. Mechanistically, UNI66 was found to interact with and inhibit BRD4 protein binding to the promoters of
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