ArticleFrontiers in cell and developmental biology2021
Oncogenic Landscape of Somatic Mutations Perturbing Pan-Cancer lncRNA-ceRNA Regulation.
Article in Frontiers in cell and developmental biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 22 citations in OpenAlex.
- A Unique Chimeric RNA: ERCC1-iASPP Drives Benzo[a]pyrene-Induced Lung Carcinogenesis via Dual Coding and Non-Coding Mechanisms.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Multi-Omics Mining of lncRNAs with Biological and Clinical Relevance in Cancer.International journal of molecular sciences · 2023Review
- Article
- Long noncoding RNA LIPH-4 promotes esophageal squamous cell carcinoma progression by regulating the miR-216b/IGF2BP2 axis.Biomarker research · 2022Article
- Stemness-related gene signature for predicting therapeutic response in patients with esophageal cancer.Translational cancer research · 2022Article
- LncRNA-IMAT1 Promotes Invasion of Meningiomas by Suppressing KLF4/hsa-miR22-3p/Snai1 Pathway.Molecules and cells · 2022Article
- Long Non-Coding RNAs Might Regulate Phenotypic Switch of Vascular Smooth Muscle Cells Acting as ceRNA: Implications for In-Stent Restenosis.International journal of molecular sciences · 2022Article
- A new pyroptosis-related signature for predicting the immune status and injury of liver ischemia-reperfusion.American journal of translational research · 2022Article
- Long non-coding RNA lncHUPC1 induced by FOXA1 promotes tumor progression by inhibiting apoptosis via miR-133b/SDCCAG3 in prostate cancer.American journal of cancer research · 2022Article
- Regulatory role of miRNAs in Wnt signaling pathway linked with cardiovascular diseases.Current research in pharmacology and drug discovery · 2022Article
- Identification of Mutation Landscape and Immune Cell Component for Liver Hepatocellular Carcinoma Highlights Potential Therapeutic Targets and Prognostic Markers.Frontiers in genetics · 2021Article
- Characterizing the Copy Number Variation of Non-Coding RNAs Reveals Potential Therapeutic Targets and Prognostic Markers of LUSC.Frontiers in genetics · 2021Article
- Integrating Genetic and Transcriptomic Data to Reveal Pathogenesis and Prognostic Markers of Pancreatic Adenocarcinoma.Frontiers in genetics · 2021Article
- Network Integration Analysis and Immune Infiltration Analysis Reveal Potential Biomarkers for Primary Open-Angle Glaucoma.Frontiers in cell and developmental biology · 2021Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Competing endogenous RNAs (ceRNA) are transcripts that communicate with and co-regulate each other by competing for the binding of shared microRNAs (miRNAs). Long non-coding RNAs (lncRNAs) as a type of ceRNA constitute a competitive regulatory network determined by miRNA response elements (MREs). Mutations in lncRNA MREs destabilize their original regulatory pathways. Study of the effects of lncRNA somatic mutations on ceRNA mechanisms can clarify tumor mechanisms and contribute to the development of precision medicine. Here, we used somatic mutation profiles collected from TCGA to characterize the role of lncRNA somatic mutations in the ceRNA regulatory network in 33 cancers. The 31,560 mutation sites identified by TargetScan and miRanda affected the balance of 70,811 ceRNA regulatory pathways. Putative mutations were categorized as high or low based on mutation frequencies. Multivariate multiple regression revealed a significant effect of 162 high-frequency mutations in six cancer types on the expression levels of target mRNAs (ceMs) through the ceRNA mechanism. Low-frequency mutations in multiple cancers perturbing 1624 ceM have been verified by Student's
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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 Socratic graph.