Evidence map›Paper›PMID 38835016›Full record

ArticleBMC biology2024

ARID1A loss promotes RNA editing of CDK13 in an ADAR1-dependent manner.

Tianyu Zhu, Qian Li, Zhe Zhang, Jiahao Shi, Yongyun Li, Feng Zhang, Lingjie Li, Xin Song, Jianfeng Shen, Renbing Jia

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in BMC biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Article
  2. Evolution of Engineered ADAR-Based RNA Editing Systems.International journal of molecular sciences · 2026
    Review
  3. Review
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

10 authors.

Tianyu Zhu *Department of Ophthalmology, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, P.R. China.
Qian Li *Department of Ophthalmology, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, P.R. China.
Zhe Zhang *Department of Ophthalmology, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, P.R. China.
Jiahao ShiDepartment of Ophthalmology, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, P.R. China.
Yongyun LiDepartment of Ophthalmology, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, P.R. China.
Feng ZhangDepartment of Histoembryology, Genetics and Developmental Biology, Shanghai Key Laboratory of Reproductive Medicine, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai, P.R. China.
Lingjie LiDepartment of Histoembryology, Genetics and Developmental Biology, Shanghai Key Laboratory of Reproductive Medicine, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai, P.R. China.
Xin SongDepartment of Ophthalmology, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, P.R. China. drsongxin_eye@163.com.
Jianfeng ShenDepartment of Ophthalmology, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, P.R. China. jfshen@shsmu.edu.cn.
Renbing JiaDepartment of Ophthalmology, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, P.R. China. renbingjia@sjtu.edu.cn.

Funding

General Program of National Natural Science Foundation of China 81972667National Key R&D Program of China 2021YFC2701103Shanghai Key Clinical Specialty, Shanghai Eye Disease Research Center 2022ZZ01003
6 · The paper itself

Abstract

backgroundARID1A, a subunit of the SWI/SNF chromatin remodeling complex, is thought to play a significant role both in tumor suppression and tumor initiation, which is highly dependent upon context. Previous studies have suggested that ARID1A deficiency may contribute to cancer development. The specific mechanisms of whether ARID1A loss affects tumorigenesis by RNA editing remain unclear.

resultsOur findings indicate that the deficiency of ARID1A leads to an increase in RNA editing levels and alterations in RNA editing categories mediated by adenosine deaminases acting on RNA 1 (ADAR1). ADAR1 edits the CDK13 gene at two previously unidentified sites, namely Q113R and K117R. Given the crucial role of CDK13 as a cyclin-dependent kinase, we further observed that ADAR1 deficiency results in changes in the cell cycle. Importantly, the sensitivity of ARID1A-deficient tumor cells to SR-4835, a CDK12/CDK13 inhibitor, suggests a promising therapeutic approach for individuals with ARID1A-mutant tumors. Knockdown of ADAR1 restored the sensitivity of ARID1A deficient cells to SR-4835 treatment.

conclusionsARID1A deficiency promotes RNA editing of CDK13 by regulating ADAR1.

Indexed as

Adenosine DeaminaseCyclin-Dependent KinasesDNA-Binding ProteinsRNA-Binding ProteinsRNA EditingTranscription FactorsCDC2 Protein KinaseCell Line, TumorHumansADAR protein, humanAdenosine DeaminaseARID1A protein, humanCDC2 Protein KinaseCDK13 protein, humanCyclin-Dependent KinasesDNA-Binding ProteinsRNA-Binding ProteinsTranscription FactorsADAR1ARID1ACDK13RNA editingTumorigenesis

Identifiers

PMID38835016
PMCPMC11151582

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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.