Evidence map›Paper›PMID 28525375›Full record

ArticleOncotarget2017

ROS enhance angiogenic properties via regulation of NRF2 in tumor endothelial cells.

Takayuki Hojo, Nako Maishi, Alam Mohammad Towfik, Kosuke Akiyama, Noritaka Ohga, Masanobu Shindoh, Yasuhiro Hida, Kazuyuki Minowa, Toshiaki Fujisawa, Kyoko Hida

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

23 citing papers in PubMed, 43 citations in OpenAlex.

  1. Article
  2. Oxidative stress and serum deprivation influence the evolution of newly formed tetraploid cells during tumorigenesis.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  3. Article
  4. Article
  5. Beyond starving cancer: anti-angiogenic therapy.Journal of medical ultrasonics (2001) · 2024
    Review
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  11. AnFrontiers in genetics · 2021
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  17. Article
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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

10 authors at 1 institution in 1 country.

Takayuki HojoVascular Biology, Frontier Research Unit, Institute for Genetic Medicine, Hokkaido University, Sapporo 060-0815, Japan.
Nako MaishiVascular Biology, Frontier Research Unit, Institute for Genetic Medicine, Hokkaido University, Sapporo 060-0815, Japan.
Alam Mohammad TowfikVascular Biology, Frontier Research Unit, Institute for Genetic Medicine, Hokkaido University, Sapporo 060-0815, Japan.
Kosuke AkiyamaVascular Biology, Frontier Research Unit, Institute for Genetic Medicine, Hokkaido University, Sapporo 060-0815, Japan.
Noritaka OhgaVascular Biology, Frontier Research Unit, Institute for Genetic Medicine, Hokkaido University, Sapporo 060-0815, Japan.
Masanobu ShindohDepartment of Oral Pathology and Biology, Hokkaido University Graduate School of Dental Medicine, Sapporo 060-8586, Japan.
Yasuhiro HidaDepartment of Cardiovascular and Thoracic Surgery, Hokkaido University Graduate School of Medicine, Sapporo 060-8638, Japan.
Kazuyuki MinowaDepartment of Dental Radiology, Hokkaido University Graduate School of Dental Medicine, Sapporo 060-8586, Japan.
Toshiaki FujisawaDepartment of Dental Anesthesiology, Hokkaido University Graduate School of Dental Medicine, Sapporo 060-8586, Japan.
Kyoko HidaVascular Biology, Frontier Research Unit, Institute for Genetic Medicine, Hokkaido University, Sapporo 060-0815, Japan.
Hokkaido University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Reactive oxygen species (ROS) are unstable molecules that activate oxidative stress. Because of the insufficient blood flow in tumors, the tumor microenvironment is often exposed to hypoxic condition and nutrient deprivation, which induces ROS accumulation. We isolated tumor endothelial cells (TECs) and found that they have various abnormalities, although the underlying mechanisms are not fully understood. Here we showed that ROS were accumulated in tumor blood vessels and ROS enhanced TEC migration with upregulation of several angiogenesis related gene expressions. It was also demonstrated that these genes were upregulated by regulation of Nuclear factor erythroid 2-related factor 2 (NRF2). Among these genes, we focused on Biglycan, a small leucine-rich proteoglycan. Inhibition of Toll-like receptors 2 and 4, known BIGLYCAN (BGN) receptors, cancelled the TEC motility stimulated by ROS. ROS inhibited NRF2 expression in TECs but not in NECs, and NRF2 inhibited phosphorylation of SMAD2/3, which activates transcription of BGN. These results indicated that ROS-induced BGN caused the pro-angiogenic phenotype in TECs via NRF2 dysregulation.

Indexed as

BiglycanCell Line, TumorCell MovementEndothelial CellsGene Expression Regulation, NeoplasticHumansNeoplasmsNeovascularization, PathologicNF-E2-Related Factor 2Oxidative StressReactive Oxygen SpeciesSmad2 ProteinSmad3 ProteinBiglycanNF-E2-Related Factor 2Reactive Oxygen SpeciesSmad2 ProteinSmad3 Proteinbiglycannuclear factor erythroid 2-related factor 2reactive oxygen speciestumor angiogenesistumor endothelial cells

Identifiers

PMID28525375
PMCPMC5542202
OpenAlexW2611679726

What OpenQuestion holds

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LicenceCC BY
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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.