Evidence map›Paper›PMID 26297045›Full record

ArticleJournal of neuro-oncology2015

Reactive oxygen species production has a critical role in hypoxia-induced Stat3 activation and angiogenesis in human glioblastoma.

Mi Ok Yu, Kyung-Jae Park, Dong-Hyuk Park, Yong-Gu Chung, Sung-Gil Chi, Shin-Hyuk Kang

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of neuro-oncology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.2field-weighted citation impact, top 11% 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

21 citing papers in PubMed, 34 citations in OpenAlex.

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  12. The complement system in glioblastoma multiforme.Acta neuropathologica communications · 2018
    Review
  13. Article
  14. Article
  15. Epigenetics of Mucus Hypersecretion in Chronic Respiratory Diseases.American journal of respiratory cell and molecular biology · 2018
    Review
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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

6 authors at 1 institution in 1 country.

Mi Ok YuDepartment of Neurosurgery, College of Medicine, Korea University, #126, 5-ga, Anam-Dong, Seongbuk-Gu, Seoul, 136-705, Korea.
Kyung-Jae ParkDepartment of Neurosurgery, College of Medicine, Korea University, #126, 5-ga, Anam-Dong, Seongbuk-Gu, Seoul, 136-705, Korea.
Dong-Hyuk ParkDepartment of Neurosurgery, College of Medicine, Korea University, #126, 5-ga, Anam-Dong, Seongbuk-Gu, Seoul, 136-705, Korea.
Yong-Gu ChungDepartment of Neurosurgery, College of Medicine, Korea University, #126, 5-ga, Anam-Dong, Seongbuk-Gu, Seoul, 136-705, Korea.
Sung-Gil ChiSchool of Life Sciences and Biotechnology, Korea University, 5-1 Anam-Dong, Seongbuk-Gu, Seoul, 136-701, Korea. chi6302@korea.ac.kr.
Shin-Hyuk KangDepartment of Neurosurgery, College of Medicine, Korea University, #126, 5-ga, Anam-Dong, Seongbuk-Gu, Seoul, 136-705, Korea. hermes23@kumc.or.kr.
Korea University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioblastoma is the most aggressive primary brain tumor with hypoxia-associated morphologic features including pseudopalisading necrosis and endothelial hyperplasia. It has been known that hypoxia can activate signal transducer and activator of transcription 3 (Stat3) and subsequently induce angiogenesis. However, the molecular mechanism underlying hypoxia-induced Stat3 activation has not been defined. In this study, we explored the possible implication of reactive oxygen species (ROS) in hypoxia-driven Stat3 activation in human glioblastoma. We found that hypoxic stress increased ROS production as well as Stat3 activation and that ROS inhibitors (diphenyleneiodonium, rotenone and myxothiazol) and an antioxidant (N-acetyl-L-cysteine) blocked Stat3 activation under hypoxic conditions. To determine a major route of ROS production, we tested whether nicotinamide adenine dinucleotide phosphate oxidase 4 (Nox4) is involved in hypoxia-induced ROS production. Nox4 expression was found to be increased at both mRNA and protein levels in hypoxic glioblastoma cells. In addition, siRNA-mediated knockdown of Nox4 expression abolished hypoxia induced Stat3 activation and vascular endothelial growth factor expression, which is associated with tumor cells' ability to trigger tube formation of endothelial cells in vitro. Our findings indicate that elevated ROS production plays a crucial role for Stat3 activation and angiogenesis in hypoxic glioblastoma cells.

Indexed as

AcetylcysteineBrain NeoplasmsCell Line, TumorEnzyme InhibitorsFree Radical ScavengersGene Expression Regulation, NeoplasticGlioblastomaHumansHypoxiaNADPH Oxidase 4NADPH OxidasesNeovascularization, PathologicReactive Oxygen SpeciesRNA, MessengerRNA, Small InterferingSignal TransductionAcetylcysteineEnzyme InhibitorsFree Radical ScavengersNADPH Oxidase 4NADPH OxidasesNOX4 protein, humanReactive Oxygen SpeciesRNA, MessengerRNA, Small InterferingSTAT3 protein, humanSTAT3 Transcription FactorVascular Endothelial Growth Factor AAngiogenesisHypoxiaNADPH oxidase 4Reactive oxygen speciesSignal transducer and activator of transcription 3

Identifiers

PMID26297045
OpenAlexW1873822182

What OpenQuestion holds

Textmetadata
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.