Evidence map›Paper›PMID 39825637›Full record

ArticleCNS neuroscience & therapeutics2025

ADAR1 Promotes the Progression and Temozolomide Resistance of Glioma Through p62-Mediated Selective Autophagy.

Yuyan Zhang, Huiling Guo, Jiahao Bu, Weiwei Wang, Li Wang, Zhibo Liu, Yuning Qiu, Qimeng Wang, Lijuan Zhou, Xianzhi Liu and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in CNS neuroscience & therapeutics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

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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

5 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Targeting RNA adenosine editing and modification enzymes for RNA therapeutics.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Review
  5. 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

12 authors.

Yuyan ZhangDepartment of Neurosurgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.
Huiling GuoDepartment of Clinical Laboratory, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.
Jiahao BuDepartment of Neurosurgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.
Weiwei WangDepartment of Pathology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.ORCID 0000-0001-9059-3265
Li WangDepartment of Pathology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.
Zhibo LiuDepartment of Clinical Laboratory, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.
Yuning QiuDepartment of Neurosurgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.
Qimeng WangDepartment of Pathology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.
Lijuan ZhouElectron Microscopy Laboratory of Renal Pathology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.
Xianzhi LiuDepartment of Neurosurgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.
Liwei MaDepartment of Clinical Laboratory, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.
Jianwei WeiDepartment of Neurosurgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.ORCID 0009-0009-1649-0941

Funding

Foundation for Innovative Research Groups of the National Natural Science Foundation of China 82002751Henan Province Key Research and Development (R & D) program 232300421125Henan Province Outstanding Young Talent Project in Health Science and Technology Innovation for Young and Middle-aged People JQRC2024010Key project of Henan Natural Science Foundation 242300421195Key scientific research project plan of colleges and universities in Henan Province 24A320048Medical Science and Technology Project of Henan Province SBGJ202102139
6 · The paper itself

Abstract

backgroundResistance to temozolomide (TMZ) remains is an important cause of treatment failure in patients with glioblastoma multiforme (GBM). ADAR1, as a member of the ADAR family, plays an important role in cancer progression and chemotherapy resistance. However, the mechanism by which ADAR1 regulates GBM progression and TMZ resistance is still unclear.

methodsWe first constructed stable transfected strains in which ADAR1 was knocked down and overexpressed to investigate the effect of ADAR1 on the first-line glioma chemotherapy drug TMZ. Subsequently, we validated that ADAR1 induces autophagy activation and used autophagy inhibitors to suppress autophagy, demonstrating that ADAR1 enhances TMZ resistance through autophagy. We further knocked down p62 (SQSTM1) based on the overexpression of ADAR1, and the results showed that ADAR1 regulates selective autophagy through the p62 regulation. Finally, we demonstrated through mutations at both edited and nonedited sites that ADAR1 regulates selective autophagy in an edited dependent way.

resultsFurther analysis showed that in the presence of TMZ, elevated ADAR1 promoted TMZ induced autophagy activation. Further research revealed that ADAR1 enhances TMZ resistance through p62-mediated selective autophagy. Further, ADAR1 regulates selective autophagy in an edited dependent way. Our results indicate a relationship between ADAR1 levels and the response of glioma patients to TMZ treatment.

conclusionsWe found that the expression of ADAR1 is upregulated in GBM and is associated with tumor grade and TMZ resistance. Elevated expression of ADAR1 predicts poor prognosis in GBM patients and promotes tumor growth in vivo or in vitro.

Indexed as

Adenosine DeaminaseAntineoplastic Agents, AlkylatingAutophagyBrain NeoplasmsDrug Resistance, NeoplasmGliomaRNA-Binding ProteinsSequestosome-1 ProteinTemozolomideAnimalsCell Line, TumorDisease ProgressionGlioblastomaHumansADAR protein, humanAdenosine DeaminaseAntineoplastic Agents, AlkylatingP62 protein, humanRNA-Binding ProteinsSequestosome-1 ProteinSQSTM1 protein, humanTemozolomideADAR1autophagygliomap62TMZ resistance

Identifiers

PMID39825637
PMCPMC11742087

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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.