ArticleNucleic acids research2025
Pyridine-bis(benzimidazole) induces DNA damage at G-quadruplex loci and promotes synthetic lethality with DNA repair inhibition.
Article in Nucleic acids research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed.
- Computer-Aided Discovery of EGFR G-Quadruplex Targeting Phenanthroimidazole Derivatives Inducing Concurrent Multi-Organelle Damage in Glioblastoma.Antioxidants (Basel, Switzerland) · 2026Article
- G-quadruplex structures as regulators of cellular processes and drivers of genome instability in cancer.Critical reviews in biochemistry and molecular biology · 2026Review
- Synthesis and biological evaluation of bisspirooxindole-hexahydroindolizines as potential anticancer agent.Molecular diversity · 2026Article
- Visualizing cellular G-quadruplexes with a bioinspired chemiluminescent probe.Nucleic acids research · 2026Article
- G-quadruplex stabilization via small molecules as a potential anti-cancer strategy.Cellular & molecular biology letters · 2026Review
- Natural G-Quadruplex Stabilizers: A Targeted Strategy for Breast Cancer Therapy.Drug design, development and therapy · 2026Review
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
G-quadruplexes (G4s) are noncanonical DNA structures that play key roles in regulating replication, transcription, and genome stability. Here, we investigate the effects of pyridine-bis(benzimidazole) (PyBI), a selective parallel and hybrid G4 stabilizer, on genome stability in cells. Biophysical and biochemical assays confirm PyBI's strong affinity for parallel G4s, leading to replication fork stalling and transcriptional repression of G4-associated oncogenes. Cleavage under targets and tagmentation (CUT&Tag) sequencing reveals a PyBI-induced genome-wide increase in G4 peaks, particularly at promoter and transcription start site regions. This G4 induction and stabilization triggers replication stress, G2/M arrest, and apoptosis. DNA repair pathway profiling shows that PyBI-induced G4 stabilization activates both homologous recombination and nonhomologous end joining (NHEJ), with a predominant role for NHEJ, as indicated by higher 53BP1 colocalization at G4 sites. Genome-wide mapping of PyBI-induced DNA breaks further supports a direct link between G4 stabilization and DNA damage. Moreover, PyBI shows synthetic lethality in DNA repair-deficient contexts, highlighting its therapeutic potential. These findings provide mechanistic insights into the genotoxic effects of PyBI and highlight its potential as a novel anticancer agent targeting G4-mediated genome instability.
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Registered trials
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