Evidence map›Paper›PMID 38644551›Full record

ArticleCNS neuroscience & therapeutics2024

USP19 regulates DNA methylation damage repair and confers temozolomide resistance through MGMT stabilization.

Jiaqi Liu, Kaikai Wang, Qian Zhu, Yixin Zhang, Yuping Chen, Zhenkun Lou, Jian Yuan

Open access · goldAbstract read
In one paragraph

Article in CNS neuroscience & therapeutics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
3.1field-weighted citation impact, top 9% 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

10 citing papers in PubMed, 7 citations in OpenAlex.

  1. Review
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  8. HIG-2 promotes glioma stemness and radioresistance mediated by IGFBP2-rich microparticles in hypoxia.Apoptosis : an international journal on programmed cell death · 2025
    Article
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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

7 authors at 5 institutions in 2 countries.

Jiaqi LiuDepartment of Plastic and Reconstructive Surgery, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.ORCID 0009-0004-6391-7454
Kaikai WangDepartment of Neurosurgery, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China.
Qian ZhuDepartment of Radiation Oncology, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.
Yixin ZhangDepartment of Plastic and Reconstructive Surgery, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Yuping ChenState Key Laboratory of Cardiology and Research Center for Translational Medicine, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.
Zhenkun LouDepartment of Oncology, Mayo Clinic, Rochester, Minnesota, USA.
Jian YuanState Key Laboratory of Cardiology and Research Center for Translational Medicine, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.
Mayo Clinic · USShanghai East Hospital · CNRuijin Hospital · CNSecond Affiliated Hospital of Zhejiang University · CNShanghai Jiao Tong University · CN

Funding

National Natural Science Foundation of China 82002634National Natural Science Foundation of China 82203457National Natural Science Foundation of China 82225035
6 · The paper itself

Abstract

objectiveTo elucidate the relationship between USP19 and O(6)-methylguanine-DNA methyltransferase (MGMT) after temozolomide treatment in glioblastoma (GBM) patients with chemotherapy resistance.

methodsScreening the deubiquitinase pannel and identifying the deubiquitinase directly interacts with and deubiquitination MGMT. Deubiquitination assay to confirm USP19 deubiquitinates MGMT. The colony formation and tumor growth study in xenograft assess USP19 affects the GBM sensitive to TMZ was performed by T98G, LN18, U251, and U87 cell lines. Immunohistochemistry staining and survival analysis were performed to explore how USP19 is correlated to MGMT in GBM clinical management.

resultsUSP19 removes the ubiquitination of MGMT to facilitate the DNA methylation damage repair. Depletion of USP19 results in the glioblastoma cell sensitivity to temozolomide, which can be rescued by overexpressing MGMT. USP19 is overexpressed in glioblastoma patient samples, which positively correlates with the level of MGMT protein and poor prognosis in these patients.

conclusionThe regulation of MGMT ubiquitination by USP19 plays a critical role in DNA methylation damage repair and GBM patients' temozolomide chemotherapy response.

Indexed as

Antineoplastic Agents, AlkylatingDNA MethylationDNA Modification MethylasesDNA Repair EnzymesDrug Resistance, NeoplasmTemozolomideTumor Suppressor ProteinsAnimalsBrain NeoplasmsCell Line, TumorDacarbazineDNA RepairEndopeptidasesFemaleGlioblastomaHumansAntineoplastic Agents, AlkylatingDacarbazineDNA Modification MethylasesDNA Repair EnzymesEndopeptidasesMGMT protein, humanTemozolomideTumor Suppressor ProteinsdeubiquitinationglioblastomaMGMTtemozolomide resistenceusp19

Identifiers

PMID38644551
PMCPMC11033335
OpenAlexW4395009515

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.