ArticleScientific reports2025
The effect of prolonged G-quadruplex stabilization on the functions of human cells.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- G-quadruplex structures as regulators of cellular processes and drivers of genome instability in cancer.Critical reviews in biochemistry and molecular biology · 2026Review
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Authors and funding
9 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Guanine-rich DNA sequences have a propensity to form G-quadruplex structures. These structures play several important biological roles and are potential targets for anticancer drugs. However, no G-quadruplex-stabilizing agent has yet been approved for clinical use. Given that G-quadruplex stabilization is quite promising as a mechanism for novel anticancer therapies, it is crucial to elucidate its effects on healthy human cells. In our study, we modeled a potential human treatment using G4 -stabilizing agents and analyzed their effects on genome integrity, transcriptomic changes, and mitochondrial function focusing on non-cancerous cells to predict potential side effects of such treatments. We found that G-quadruplex stabilization does not compromise genome integrity. However, it can induce persistent alterations in the transcriptomic profile of human cells, including genes encoded on the mitochondrial genome. Notably, certain G-quadruplex-stabilizing agents triggered mitophagy in both human cells and Drosophila melanogaster. In summary, our findings indicate that while G-quadruplex stabilization does not cause genome instability, it may pose potential risks due to its long-term effects on transcription and its ability to induce mitophagy. Therefore, we recommend that all potential drug candidates be thoroughly evaluated for their ability to induce mitophagy and to promote cancer formation in animal models prior to clinical trials.
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