Evidence map›Paper›PMID 34496885›Full record

ArticleMolecular cancer2021

An ADAR1-dependent RNA editing event in the cyclin-dependent kinase CDK13 promotes thyroid cancer hallmarks.

Julia Ramírez-Moya, Christos Miliotis, Allison R Baker, Richard I Gregory, Frank J Slack, Pilar Santisteban

Open access · goldAbstract read
In one paragraph

Article in Molecular cancer, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
4.1field-weighted citation impact, top 5% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

45 citing papers in PubMed, 63 citations in OpenAlex.

  1. Review
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  16. ADARp110 promotes hepatocellular carcinoma progression via stabilization of CD24 mRNA.Proceedings of the National Academy of Sciences of the United States of America · 2025
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 2 countries.

Julia Ramírez-MoyaInstituto, de Investigaciones Biomédicas "Alberto Sols"; Consejo Superior de Investigaciones Científicas (CSIC), Universidad Autónoma de Madrid (UAM), Madrid, Spain.ORCID 0000-0002-2458-2186
Christos MiliotisDepartment of Pathology, Harvard Medical School Initiative for RNA Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Allison R BakerDepartment of Pathology, Harvard Medical School Initiative for RNA Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Richard I GregoryStem Cell Program, Division of Hematology/Oncology, Boston Children's Hospital, Departments of Biological Chemistry and Molecular Pharmacology, and Pediatrics, Harvard Medical School, Harvard Medical School Initiative for RNA Medicine, Boston, MA, USA.
Frank J SlackDepartment of Pathology, Harvard Medical School Initiative for RNA Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA. fslack@bidmc.harvard.edu.
Pilar SantistebanInstituto, de Investigaciones Biomédicas "Alberto Sols"; Consejo Superior de Investigaciones Científicas (CSIC), Universidad Autónoma de Madrid (UAM), Madrid, Spain. psantisteban@iib.uam.es.ORCID 0000-0002-2758-796X
Beth Israel Deaconess Medical Center · USBoston Children's Hospital · USInstituto de Salud Carlos III · ES

Funding

Precision microRNA medicine in cancerR35CA232105 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI SLACK, FRANK J. · 2019 to 2025
$7.2M
Role of the Epitranscriptome in CancerR35CA232115 · NCI · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI GREGORY, RICHARD I. · 2019 to 2025
$7.2M
NCI NIH HHS R35 CA232105NCI NIH HHS R35 CA232115NIH HHS R35 CA232105
6 · The paper itself

Abstract

backgroundAdenosine deaminases acting on RNA (ADARs) modify many cellular RNAs by catalyzing the conversion of adenosine to inosine (A-to-I), and their deregulation is associated with several cancers. We recently showed that A-to-I editing is elevated in thyroid tumors and that ADAR1 is functionally important for thyroid cancer cell progression. The downstream effectors regulated or edited by ADAR1 and the significance of ADAR1 deregulation in thyroid cancer remain, however, poorly defined.

methodsWe performed whole transcriptome sequencing to determine the consequences of ADAR1 deregulation for global gene expression, RNA splicing and editing. The effects of gene silencing or RNA editing were investigated by analyzing cell viability, proliferation, invasion and subnuclear localization, and by protein and gene expression analysis.

resultsWe report an oncogenic function for CDK13 in thyroid cancer and identify a new ADAR1-dependent RNA editing event that occurs in the coding region of its transcript. CDK13 was significantly over-edited (c.308A > G) in tumor samples and functional analysis revealed that this editing event promoted cancer cell hallmarks. Finally, we show that CDK13 editing increases the nucleolar abundance of the protein, and that this event might explain, at least partly, the global change in splicing produced by ADAR1 deregulation.

conclusionsOverall, our data support A-to-I editing as an important pathway in cancer progression and highlight novel mechanisms that might be used therapeutically in thyroid and other cancers.

Indexed as

Gene Expression Regulation, NeoplasticRNA EditingAdenosine DeaminaseAllelesCDC2 Protein KinaseCell Line, TumorCell MovementCell ProliferationCell SurvivalDisease ProgressionGene Knockdown TechniquesGene SilencingHumansProtein TransportRNA-Binding ProteinsRNA SplicingADAR protein, humanAdenosine DeaminaseCDC2 Protein KinaseCDK13 protein, humanRNA-Binding ProteinsADAR1A-to-I editingCancerCDK13Splicing

Identifiers

PMID34496885
PMCPMC8424981
OpenAlexW3197046964

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.