ArticleNature communications2023
Tumour mutations in long noncoding RNAs enhance cell fitness.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 12 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
12 citing papers in PubMed, 21 citations in OpenAlex.
- Exploring the Clinical Landscape of Long Non-coding RNAs in Cancer Diagnosis and Therapy.Biochemical genetics · 2026Review
- A Modular and Programmable Cas13d Platform for RNA Single Nucleotide Variant Detection.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- LncDARS-AS1 Regulates ATP1A1 Stability and Enhances NaAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Immiscible proteins compete for RNA binding to order condensate layers.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Cancer driver topologically associated domains identify oncogenic and tumor-suppressive lncRNAs.Genome research · 2025Article
- POCALI: Prediction and Insight on CAncer LncRNAs by Integrating Multi-Omics Data with Machine Learning.Small methods · 2025Article
- Unraveling the anti-tumor effects of midazolam in non-small cell lung cancer through the lncRNA XLOC_010706/miR-520d-5p/STAT3/autophagy pathway.Scientific reports · 2025Article
- Genome biology of long non-coding RNAs in humans: A virtual karyotype.Computational and structural biotechnology journal · 2025Article
- Targeting and engineering long non-coding RNAs for cancer therapy.Nature reviews. Genetics · 2024Review
- Cell type specific long non-coding RNA targets identified by integrative analysis of single-cell and bulk colorectal cancer transcriptomes.Scientific reports · 2024Article
- Multi-Omics Mining of lncRNAs with Biological and Clinical Relevance in Cancer.International journal of molecular sciences · 2023Review
- Long Non-Coding RNAs as "MYC Facilitators".Pathophysiology : the official journal of the International Society for Pathophysiology · 2023Review
Corrections and comments
- Erratum issued
Authors and funding
33 authors at 4 institutions in 5 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Long noncoding RNAs (lncRNAs) are linked to cancer via pathogenic changes in their expression levels. Yet, it remains unclear whether lncRNAs can also impact tumour cell fitness via function-altering somatic "driver" mutations. To search for such driver-lncRNAs, we here perform a genome-wide analysis of fitness-altering single nucleotide variants (SNVs) across a cohort of 2583 primary and 3527 metastatic tumours. The resulting 54 mutated and positively-selected lncRNAs are significantly enriched for previously-reported cancer genes and a range of clinical and genomic features. A number of these lncRNAs promote tumour cell proliferation when overexpressed in in vitro models. Our results also highlight a dense SNV hotspot in the widely-studied NEAT1 oncogene. To directly evaluate the functional significance of NEAT1 SNVs, we use in cellulo mutagenesis to introduce tumour-like mutations in the gene and observe a significant and reproducible increase in cell fitness, both in vitro and in a mouse model. Mechanistic studies reveal that SNVs remodel the NEAT1 ribonucleoprotein and boost subnuclear paraspeckles. In summary, this work demonstrates the utility of driver analysis for mapping cancer-promoting lncRNAs, and provides experimental evidence that somatic mutations can act through lncRNAs to enhance pathological cancer cell fitness.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.