Evidence map›Paper›PMID 32526700›Full record

ArticleRedox biology2020

C/EBPβ mediates NQO1 and GSTP1 anti-oxidative reductases expression in glioblastoma, promoting brain tumor proliferation.

Kecheng Lei, Yiyuan Xia, Xiao-Chuan Wang, Eun Hee Ahn, Lingjing Jin, Keqiang Ye

Open access · goldAbstract read
In one paragraph

Article in Redox biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

33 citing papers in PubMed, 44 citations in OpenAlex.

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  17. Impact of NQO1 dysregulation in CNS disorders.Journal of translational medicine · 2024
    Review
  18. Article
  19. Article
  20. Article
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.

Kecheng LeiDepartment of Pathology and Laboratory Medicine, Emory University School of Medicine, Atlanta, GA, USA; Neurotoxin Research Center of Key Laboratory of Spine and Spinal Cord Injury Repair and Regeneration of Ministry of Education, Neurological Department of Tongji Hospital, Tongji University School of Medicine, 200065, Shanghai, China.
Yiyuan XiaDepartment of Pathology and Laboratory Medicine, Emory University School of Medicine, Atlanta, GA, USA; Department of Pathophysiology, Key Laboratory of Ministry of Education of Neurological Diseases, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
Xiao-Chuan WangDepartment of Pathophysiology, Key Laboratory of Ministry of Education of Neurological Diseases, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
Eun Hee AhnDepartment of Pathology and Laboratory Medicine, Emory University School of Medicine, Atlanta, GA, USA.
Lingjing JinNeurotoxin Research Center of Key Laboratory of Spine and Spinal Cord Injury Repair and Regeneration of Ministry of Education, Neurological Department of Tongji Hospital, Tongji University School of Medicine, 200065, Shanghai, China. Electronic address: lingjingjin@163.com.
Keqiang YeDepartment of Pathology and Laboratory Medicine, Emory University School of Medicine, Atlanta, GA, USA. Electronic address: kye@emory.edu.
Emory University · USHuazhong University of Science and Technology · CNTongji Hospital · CN

Funding

Molecular Mechanisms of G5-7 Allosteric Inhibition of Jak2R01CA186918 · NCI · EMORY UNIVERSITY · PI YE, KEQIANG · 2015 to 2019
$1.8M
NCI NIH HHS R01 CA186918
6 · The paper itself

Abstract

Glioblastoma (GBM) is the most common and most aggressive brain tumor, associated with high levels of reactive oxidative species (ROS) due to metabolic and signaling aberrations. High ROS levels are detrimental to cells, but it remains incompletely understood how cancer cells cope with the adverse effects. Here we show that C/EBPβ, a ROS responsive transcription factor, regulates the transcription of NQO1 and GSTP1, two antioxidative reductases, which neutralize ROS in the GBM and mediates their proliferation. C/EBPβ is upregulated in EGFR overexpressed GBM cells, inversely correlated with the survival rates of brain tumor patients. Interestingly, C/EBPβ binds the promoters of NQO1 and GSTP1 and escalates their expression. Overexpression of C/EBPβ selectively decreases the ROS in EGFR-overexpressed U87MG cells and promotes cell proliferation via upregulating NQO1 and GSTP1; whereas knocking down C/EBPβ elevates the ROS and reduces proliferation by repressing the reductases. Accordingly, C/EBPβ mediates the brain tumor growth in vivo, coupling with NQO1 and GSTP1 expression and ROS levels. Hence, C/EBPβ regulates the expression of antioxidative reductases and balances the ROS, promoting brain tumor proliferation.

Indexed as

Brain NeoplasmsGlioblastomaCCAAT-Enhancer-Binding Protein-betaCell Line, TumorCell ProliferationGlutathione S-Transferase piHumansNAD(P)H Dehydrogenase (Quinone)OxidoreductasesCCAAT-Enhancer-Binding Protein-betaCEBPB protein, humanGlutathione S-Transferase piGSTP1 protein, humanNAD(P)H Dehydrogenase (Quinone)NQO1 protein, humanOxidoreductasesC/EBPβGBMGSTP1NQO1Oxidative stressTranscription factor

Identifiers

PMID32526700
PMCPMC7287278
OpenAlexW3027556675

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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.