Evidence map›Paper›PMID 31300060›Full record

ArticleJournal of neuroinflammation2019

CCAAT/enhancer-binding protein delta regulates the stemness of glioma stem-like cells through activating PDGFA expression upon inflammatory stimulation.

Shao-Ming Wang, Hong-Yi Lin, Yen-Lin Chen, Tsung-I Hsu, Jian-Ying Chuang, Tzu-Jen Kao, Chiung-Yuan Ko

Open access · goldAbstract read
In one paragraph

Article in Journal of neuroinflammation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

19 citing papers in PubMed, 27 citations in OpenAlex.

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  13. Single-cell RNA profiling ofFrontiers in cellular and infection microbiology · 2022
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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 3 institutions in 1 country.

Shao-Ming WangGraduate Institute of Neural Regenerative Medicine, College of Medical Science and Technology, Taipei Medical University, Taipei, Taiwan.
Hong-Yi LinPh.D. Program for Neural Regenerative Medicine, College of Medical Science and Technology, Taipei Medical University and National Health Research Institutes, Taipei, Taiwan.
Yen-Lin ChenDepartment of Pathology, Cardinal Tien Hospital, School of Medicine College of Medicine, Fu Jen Catholic University, New Taipei City, Taiwan.
Tsung-I HsuGraduate Institute of Neural Regenerative Medicine, College of Medical Science and Technology, Taipei Medical University, Taipei, Taiwan.
Jian-Ying ChuangGraduate Institute of Neural Regenerative Medicine, College of Medical Science and Technology, Taipei Medical University, Taipei, Taiwan.
Tzu-Jen KaoGraduate Institute of Neural Regenerative Medicine, College of Medical Science and Technology, Taipei Medical University, Taipei, Taiwan.
Chiung-Yuan KoGraduate Institute of Neural Regenerative Medicine, College of Medical Science and Technology, Taipei Medical University, Taipei, Taiwan. ko680108@tmu.edu.tw.
Taipei Medical University · TWFu Jen Catholic University · TWNational Health Research Institutes · TW

Funding

Ministry of Education The Featured Areas Research Center Program within the frameworkMinistry of Science and Technology, Taiwan MOST 105-2320-B-038-068-MY2Ministry of Science and Technology, Taiwan MOST 107-2320-B-038-068-002Taipei Medical University Hospital TMU105-AE1-B07
6 · The paper itself

Abstract

backgroundThe small population of glioma stem-like cells (GSCs) contributes to tumor initiation, malignancy, and recurrence in glioblastoma. However, the maintenance of GSC properties in the tumor microenvironment remains unclear. In glioma, non-neoplastic cells create an inflammatory environment and subsequently mediate tumor progression and maintenance. Transcriptional factor CCAAT/enhancer-binding protein delta (CEBPD) is suggested to regulate various genes responsive to inflammatory cytokines, thus prompting us to investigate its role in regulating GSCs stemness after inflammatory stimulation.

methodsStemness properties were analyzed by using spheroid formation. Oncomine and TCGA bioinformatic databases were used to analyze gene expression. Western blotting, quantitative real-time polymerase chain reaction, luciferase reporter assay, and chromatin immunoprecipitation assay were used to analyze proteins and gene transcript levels. The glioma tissue microarrays were used for CEBPD and PDGFA expression by immunohistochemistry staining.

resultsWe first found that IL-1β promotes glioma spheroid formation and is associated with elevated CEBPD expression. Using microarray analysis, platelet-derived growth factor subunit A (PDGFA) was confirmed as a CEBPD-regulated gene that mediates IL-1β-enhanced GSCs self-renewal. Further analysis of the genomic database and tissue array revealed that the expression levels between CEBPD and PDGFA were coincident in glioma patient samples.

conclusionThis is the first report showing the activation of PDGFA expression by CEBPD through IL-1β treatment and a novel CEBPD function in maintaining the self-renewal feature of GSCs.

Indexed as

CCAAT-Enhancer-Binding Protein-deltaCell Line, TumorGene Expression Regulation, NeoplasticGliomaHumansInflammationInterleukin-1betaNeoplastic Stem CellsPlatelet-Derived Growth FactorCCAAT-Enhancer-Binding Protein-deltaCEBPD protein, humanIL1B protein, humanInterleukin-1betaPlatelet-Derived Growth Factorplatelet-derived growth factor ACEBPDGlioblastoma multiformeGlioma stem-like cellInflammationInterleukin-1βPDGFA

Identifiers

PMID31300060
PMCPMC6626372
OpenAlexW2959736753

What OpenQuestion holds

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LicenceCC BY
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.