Evidence map›Paper›PMID 39664566›Full record

ArticleInternational journal of biological sciences2024

BRD7 enhances the radiosensitivity of nasopharyngeal carcinoma cells by negatively regulating USP5/METTL3 axis-mediated homologous recombination repair.

Mengna Li, Jianxia Wei, Changning Xue, Shipeng Chen, Xiangting Zhou, Lemei Zheng, Yumei Duan, Hongyu Deng, Songqing Fan, Wei Xiong and 2 more

Abstract read
In one paragraph

Article in International journal of biological sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing 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

13 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Targeting O-GlcNAcylated METTL3 impedes MDS/AML progression via diminishing SRSF1 mMolecular therapy : the journal of the American Society of Gene Therapy · 2025
    Article
  10. O-GlcNAcylation locks the m6A-SRSF1-MCL1 axis in myeloid malignancies.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Article
  11. Article
  12. Review
  13. 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.

Mengna LiNHC Key Laboratory of Carcinogenesis, Hunan Key Laboratory of Oncotarget Gene, Hunan Cancer Hospital/the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha 410078, China.
Jianxia WeiNHC Key Laboratory of Carcinogenesis, Hunan Key Laboratory of Oncotarget Gene, Hunan Cancer Hospital/the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha 410078, China.
Changning XueNHC Key Laboratory of Carcinogenesis, Hunan Key Laboratory of Oncotarget Gene, Hunan Cancer Hospital/the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha 410078, China.
Shipeng ChenNHC Key Laboratory of Carcinogenesis, Hunan Key Laboratory of Oncotarget Gene, Hunan Cancer Hospital/the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha 410078, China.
Xiangting ZhouNHC Key Laboratory of Carcinogenesis, Hunan Key Laboratory of Oncotarget Gene, Hunan Cancer Hospital/the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha 410078, China.
Lemei ZhengNHC Key Laboratory of Carcinogenesis, Hunan Key Laboratory of Oncotarget Gene, Hunan Cancer Hospital/the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha 410078, China.
Yumei DuanNHC Key Laboratory of Carcinogenesis, Hunan Key Laboratory of Oncotarget Gene, Hunan Cancer Hospital/the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha 410078, China.
Hongyu DengNHC Key Laboratory of Carcinogenesis, Hunan Key Laboratory of Oncotarget Gene, Hunan Cancer Hospital/the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha 410078, China.
Songqing FanDepartment of Pathology, the Second Xiangya Hospital, Central South University, Changsha 410011, China.
Wei XiongNHC Key Laboratory of Carcinogenesis, Hunan Key Laboratory of Oncotarget Gene, Hunan Cancer Hospital/the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha 410078, China.
Faqing TangNHC Key Laboratory of Carcinogenesis, Hunan Key Laboratory of Oncotarget Gene, Hunan Cancer Hospital/the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha 410078, China.
Ming ZhouNHC Key Laboratory of Carcinogenesis, Hunan Key Laboratory of Oncotarget Gene, Hunan Cancer Hospital/the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha 410078, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

An important reason for the poor prognosis of nasopharyngeal carcinoma (NPC) patients is radioresistance. Our previous studies demonstrated that BRD7 is expressed at low levels in NPC and functions as a tumor suppressor to inhibit NPC progression and metastasis. However, the role and mechanism of BRD7 in the development of radioresistance in NPC cells remain unclear. In this study, we first found that BRD7 was lowly expressed in radioresistant NPC tissues and cells compared to radiosensitive tissues and cells and that overexpression of BRD7 promoted the induction of DNA double-strand breaks and increased radiosensitivity in NPC cells. Mechanistically, BRD7 competitively inhibits the binding of the deubiquitinating enzyme USP5 to METTL3, thereby reducing the protein stability of METTL3 through the ubiquitin-proteasome pathway. Furthermore, METTL3 was confirmed to suppress the induction of DSBs and promote the development of NPC radioresistance by regulating BRCA1- and RAD51-mediated homologous recombination repair. Moreover, high BRD7 expression and low METTL3 expression are positively correlated with radiosensitivity and good prognosis in NPC patients. Taken together, our findings reveal that BRD7 promotes the radiosensitization of NPC cells by negatively regulating USP5/METTL3 axis activity and indicate that targeting the BRD7/METTL3 axis might be a novel therapeutic strategy for NPC radiosensitization.

Indexed as

MethyltransferasesNasopharyngeal CarcinomaNasopharyngeal NeoplasmsRadiation ToleranceRecombinational DNA RepairBromodomain Containing ProteinsCell Line, TumorChromosomal Proteins, Non-HistoneGene Expression Regulation, NeoplasticHumansUbiquitin-Specific ProteasesBRD7 protein, humanBromodomain Containing ProteinsChromosomal Proteins, Non-HistoneMethyltransferasesMETTL3 protein, humanUbiquitin-Specific ProteasesBRD7METTL3Nasopharyngeal carcinomaRadiosensitivityUbiquitin-proteasome.USP5

Identifiers

PMID39664566
PMCPMC11628346

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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.