Evidence map›Paper›PMID 31485609›Full record

ArticleInternational journal of oncology2019

Bromodomain inhibitor jq1 induces cell cycle arrest and apoptosis of glioma stem cells through the VEGF/PI3K/AKT signaling pathway.

Naiyan Wen, Baofeng Guo, Hongwu Zheng, Libo Xu, Hang Liang, Qian Wang, Ding Wang, Xuyang Chen, Shengnan Zhang, Yang Li and 1 more

Open access · hybridAbstract read
In one paragraph

Article in International journal of oncology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

59 citing papers in PubMed, 80 citations in OpenAlex.

  1. Review
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  4. Targeting BRD4-A Promising Therapeutic Option for Glioblastoma?International journal of molecular sciences · 2026
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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

11 authors at 4 institutions in 2 countries.

Naiyan WenDepartment of Pathophysiology, College of Basic Medical Sciences, Jilin University, Changchun, Jilin 130021, P.R. China.
Baofeng GuoDepartment of Plastic Surgery, China‑Japan Union Hospital, Jilin University, Changchun, Jilin 130033, P.R. China.
Hongwu ZhengDepartment of Pathology and Laboratory Medicine, Weill Cornell Medicine, New York, NY 10065, USA.
Libo XuDepartment of Pathophysiology, College of Basic Medical Sciences, Jilin University, Changchun, Jilin 130021, P.R. China.
Hang LiangDepartment of Pathophysiology, College of Basic Medical Sciences, Jilin University, Changchun, Jilin 130021, P.R. China.
Qian WangDepartment of Pathophysiology, College of Basic Medical Sciences, Jilin University, Changchun, Jilin 130021, P.R. China.
Ding WangDepartment of Pathophysiology, College of Basic Medical Sciences, Jilin University, Changchun, Jilin 130021, P.R. China.
Xuyang ChenDepartment of Pathophysiology, College of Basic Medical Sciences, Jilin University, Changchun, Jilin 130021, P.R. China.
Shengnan ZhangDepartment of Pathophysiology, College of Basic Medical Sciences, Jilin University, Changchun, Jilin 130021, P.R. China.
Yang LiDepartment of Pathophysiology, College of Basic Medical Sciences, Jilin University, Changchun, Jilin 130021, P.R. China.
Ling ZhangDepartment of Pathophysiology, College of Basic Medical Sciences, Jilin University, Changchun, Jilin 130021, P.R. China.
Jilin University · CNJilin Medical University · CNCornell University · USUnion Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bromodomain and extraterminal domain proteins, especially bromodomain‑containing protein 4 (Brd4), have recently emerged as therapeutic targets for several cancers, although the role and mechanism of Brd4 in glioblastoma multiforme (GBM) are unclear. In this study, we aimed to explore the underlying mechanisms of the anti‑tumor effects of Brd4 and the bromodomain inhibitor JQ1 on glioma stem cells (GSCs). In vitro, JQ1 and small interfering RNAs targeting Brd4 (siBrd4) inhibited the proliferation and self‑renewal of GSCs. In vivo, JQ1 significantly inhibited the growth of xenograft GSCs tumors. The RNA‑seq analysis revealed that the PI3K‑AKT pathway played an important role in GBM. Vascular endothelial growth factor (VEGF) and VEGF receptor 2 phosphorylation was downregulated by exposure to JQ1 in GSCs, thereby reducing PI3K and AKT activity. In addition, treatment with JQ1 inhibited MMP expression, thereby inhibiting degradation of the extracellular matrix by MMP and angiogenesis in GBM tumors. Suppression of AKT phosphorylation inhibited the expression of the retinoblastoma/E2F1 complex, resulting in cell cycle arrest. In addition, treatment with siBrd4 or JQ1 induced apoptosis by activating AKT downstream target genes involved in apoptosis. In conclusion, these results suggest that Brd4 has great potential as a therapeutic target, and JQ1 has notable anti‑tumor effects against GBM which may be mediated via the VEGF/PI3K/AKT signaling pathway.

Indexed as

AnimalsAzepinesBrain NeoplasmsBromodomain Containing ProteinsCell Cycle CheckpointsCell Cycle ProteinsCell Line, TumorCell ProliferationCell SurvivalGene Expression Regulation, NeoplasticGliomaHumansMaleMiceNeoplastic Stem CellsPhosphatidylinositol 3-KinasesAzepinesBRD4 protein, humanBromodomain Containing ProteinsCell Cycle Proteins(+)-JQ1 compoundPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTranscription FactorsTriazolesVascular Endothelial Growth Factor AVEGFA protein, human

Identifiers

PMID31485609
PMCPMC6741838
OpenAlexW2970931615

What OpenQuestion holds

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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.