ArticleBMC biology2025
Pharmacomodulation of G-quadruplexes in long non-coding RNAs dysregulated in colorectal cancer.
Article in BMC biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- DNA damaging properties of G-quadruplex ligand QN-302 are potentiated by the DNA repair inhibitor Olaparib and mitigated by the molecular helicase PhpC.Genome biology · 2026Article
- Putative G‑Quadruplex Structures in Dysregulated Long Non-coding RNA of Ovarian Cancer and Their Binding Interactions with Human Serum Albumin.ACS omega · 2025Article
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Authors and funding
7 authors.
Funding
Abstract
backgroundNon-coding RNAs (ncRNAs) in human cells constitute a substantial portion of the transcriptome but do not lead to protein synthesis. Among them, long non-coding RNAs (lncRNAs, > 200 nucleotides long) are fascinating in their ability to orchestrate critical cellular functions that govern cell development, differentiation, and metabolism. Therefore, the dysregulation of lncRNAs has been linked with several diseases, chiefly cancers.
resultsWe focused here on colorectal cancer (CRC), the second-highest cause of mortalities related to cancer worldwide, and more particularly on three lncRNAs, i.e., LINC01589, MELTF-AS1, and UXT-AS1, known to be dysregulated in CRC. We identified a vulnerability in these lncRNAs that could be exploited from a therapeutic point of view: a part of their sequence folds into a secondary structure referred to as G-quadruplex (G4), which is suspected to play active roles in the lncRNA functions. We demonstrate here that these sequences do fold into G4s both in vitro and in CRC cells, and that these G4s can be modulated using PhpC, a prototype molecule for destabilizing G4s.
conclusionWe describe an innovative anticancer strategy that fully abides by the rules of chemical biology. We indeed modulate the formation of G4s in cells using ad hoc molecular tools in the aim of disturbing the homeostasis and inner functioning of lncRNAs. By exploiting cellular outcomes, we infer how this pharmacomodulation affects CRC biology and, beyond this, the fate of CRC cells owing to the flawed repertoire of correction and/or compensatory mechanisms in cancer cells.
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