Evidence map›Paper›PMID 41387767›Full record

ArticleBMC genomics2025

Associating cancer-related RNA structure disrupting SNPs in LincRNAs to function.

Xueer Han, Christian Anthon, Adrian Sven Geissler, Radhakrishnan Sabarinathan, Stefan Ernst Seemann, Jakob Hull Havgaard, Jan Gorodkin

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Article in BMC genomics, 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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1citing papers in PubMed
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1 · What the graph read from it

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3 · Its place in the literature

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1 citing paper in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

7 authors.

Xueer HanDepartment of Veterinary and Animal Sciences, Center for non-coding RNA in Technology and Health, University of Copenhagen, Copenhagen, Denmark.
Christian AnthonDepartment of Veterinary and Animal Sciences, Center for non-coding RNA in Technology and Health, University of Copenhagen, Copenhagen, Denmark.
Adrian Sven GeisslerDepartment of Veterinary and Animal Sciences, Center for non-coding RNA in Technology and Health, University of Copenhagen, Copenhagen, Denmark.
Radhakrishnan SabarinathanNational Centre for Biological Sciences, Tata Institute of Fundamental Research, Bengaluru, Karnataka, India.
Stefan Ernst SeemannDepartment of Veterinary and Animal Sciences, Center for non-coding RNA in Technology and Health, University of Copenhagen, Copenhagen, Denmark.
Jakob Hull HavgaardDepartment of Veterinary and Animal Sciences, Center for non-coding RNA in Technology and Health, University of Copenhagen, Copenhagen, Denmark. hull@rth.dk.
Jan GorodkinDepartment of Veterinary and Animal Sciences, Center for non-coding RNA in Technology and Health, University of Copenhagen, Copenhagen, Denmark. gorodkin@rth.dk.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLong intergenic non-coding RNAs (lincRNAs) and single nucleotide polymorphisms (SNPs) have been associated with cancers for years, yet the molecular mechanism is mostly unclear. The secondary structure of lincRNAs is often crucial for their biological function but can be disrupted by SNPs. However, only a small number of studies investigated how lincRNAs function through secondary structure. Given that the vast majority of cancer-related SNPs are located mainly in non-coding regions, there is a large potential for associating SNPs to disrupted structure in lincRNAs.

methodsTo estimate the structural impacts of cancer-associated SNPs on lincRNAs, we predicted local secondary structures for lincRNAs and computed structural distances between structural ensembles of the wild-type and mutant sequences. Manual literature curation was performed to study the function of lincRNAs that are structurally disrupted by cancer-associated SNPs. By integrating with RBP binding sites annotation, we estimated the impacts of structural changes from cancer-associated SNPs on the protein binding of lincRNAs.

resultsWe predict 559 SNPs to cause significant structural disruption in 231 lincRNAs using RNAsnp (P-value < 0.1). In addition, we find that these disrupted regions have the potential to alter the binding ability of lincRNAs with RBPs. An example is the structural change in the lincRNA small nucleolar RNA host gene 25 (SNHG25), which overlaps the binding site of protein insulin like growth factor 2 mRNA binding protein 2 (IGF2BP2) in glioblastoma multiforme.

conclusionsThe results show the importance of the lincRNA secondary structure in understanding their biological function, especially the structural changes from SNPs in cancer. The predicted structural change in lincRNA SNHG25 holds a potential insight into the mechanism of protein IGF2BP2 in recognizing RNA methylation signals in glioblastoma multiforme.

Indexed as

NeoplasmsPolymorphism, Single NucleotideRNA, Long NoncodingBinding SitesHumansNucleic Acid ConformationRNA-Binding ProteinsRNA-Binding ProteinsRNA, Long NoncodingHuman cancerLong intergenic non-coding RNALong non-coding RNARNA binding proteinRNA methylationRNA secondary structureSingle nucleotide polymorphismStructural disruption

Identifiers

PMID41387767
PMCPMC12701586

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.