ArticlePeerJ2020
Global RNA editome landscape discovers reduced RNA editing in glioma: loss of editing of gamma-amino butyric acid receptor alpha subunit 3 (GABRA3) favors glioma migration and invasion.
Article in PeerJ, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 17 citations in OpenAlex.
- ADAR-mediated RNA editing in CNS disorders: from pathogenic mechanisms to therapeutic opportunities.Cellular & molecular biology letters · 2026Review
- Review
- Landscape of A-I RNA editing in mouse, pig, macaque, and human brains.Nucleic acids research · 2025Article
- Genetics of cell-type-specific post-transcriptional gene regulation during human neurogenesis.American journal of human genetics · 2024Article
- Emerging Roles and Mechanisms of RNA Modifications in Neurodegenerative Diseases and Glioma.Cells · 2024Review
- Genetics of cell-type-specific post-transcriptional gene regulation during human neurogenesis.bioRxiv : the preprint server for biology · 2023Article
- Neurotransmitters: Potential Targets in Glioblastoma.Cancers · 2022Review
- ADAR3 activates NF-κB signaling and promotes glioblastoma cell resistance to temozolomide.Scientific reports · 2022Article
- Article
- Epitranscriptomic Modifications Modulate Normal and Pathological Functions in CNS.Translational stroke research · 2022Review
- The role of RNA modification in the generation of acquired drug resistance in glioma.Frontiers in genetics · 2022Review
- RNA editing of ion channels and receptors in physiology and neurological disorders.Oxford open neuroscience · 2022Review
- Aberrant Expression of ADARB1 Facilitates Temozolomide Chemoresistance and Immune Infiltration in Glioblastoma.Frontiers in pharmacology · 2022Article
- Article
- RNA Editing: A New Therapeutic Target in Amyotrophic Lateral Sclerosis and Other Neurological Diseases.International journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGliomas are the most common and lethal type of intracranial tumors. With the current treatment regime, the median survival of patients with grade IV glioma (glioblastoma/GBM) remains at 14-16 months. RNA editing modifies the function and regulation of transcripts. The development of glial tumors may be caused by altered RNA editing events.
methodsIn this study, we uncover the global RNA editome landscape of glioma patients from RNA-seq data of control, lower grade glioma (LGG) and GBM samples (
resultsA-to-I editing events were found to comprise 80% of the total editing events of which 96% were located in the Alu regions. The total RNA editing events were found to be reduced in glioma compared to control samples. More specifically, we found Gamma-aminobutyric acid type A receptor alpha3 (GABRA3) to be edited (c.1026 A-to-G; pI343M) in 73% (editing ratio 0.8) of control samples compared to LGG (28.96%; 0.47) and GBM (5.2%; 0.53) samples. GABRA3 transcript level was found to be downregulated in glioma compared to control in a grade-specific manner with GBMs having the lowest level of the transcript. Further, GABRA3 transcripts were observed to be higher in edited compared to unedited glioma samples. The transcript and protein levels of exogenously expressed gene were found to be higher for edited compared to unedited GABRA3 in glioma cells. Further, exogenously expressed edited GABRA3 inhibited migration and invasion of glioma cells efficiently but not the unedited GABRA3.
conclusionCollectively, our study discovered a reduction in RNA editing during glioma development. We further demonstrate that elevated RNA editing maintains a high level of GABRA3 RNA and protein in normal glial cells which provides a less migratory environment for the normal functioning of the brain. In contrast, the reduction in GABRA3 protein levels, due to lower stability of unedited RNA, results in the loss of function which confers an aggressive phenotype to GBM tumor.
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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.