Evidence map›Paper›PMID 35158782›Full record

ArticleCancers2022

NOX2-Induced High Glycolytic Activity Contributes to the Gain of COL5A1-Mediated Mesenchymal Phenotype in GBM.

Youngjoon Park, Minwoo Park, Junhyung Kim, Juwon Ahn, Jeongmin Sim, Ji-In Bang, Jinhyung Heo, Hyejeong Choi, Kyunggi Cho, Mihye Lee and 2 more

Open access · goldAbstract read
In one paragraph

Article in Cancers, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

10 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. From glioma gloom to immune bloom: unveiling novel immunotherapeutic paradigms-a review.Journal of experimental & clinical cancer research : CR · 2024
    Review
  5. Article
  6. Article
  7. Article
  8. NOX Dependent ROS Generation and Cell Metabolism.International journal of molecular sciences · 2023
    Review
  9. Article
  10. 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

12 authors at 2 institutions in 1 country.

Youngjoon ParkBundang CHA Medical Center, Department of Neurosurgery, CHA University, Yatap-dong 59, Seongnam 13496, Korea.
Minwoo ParkDepartment of Integrated Biomedical Science, Soonchunhyang Institute of Medi-bio Science (SIMS), Soonchunhyang University, Cheonan 31151, Korea.
Junhyung KimDepartment of Integrated Biomedical Science, Soonchunhyang Institute of Medi-bio Science (SIMS), Soonchunhyang University, Cheonan 31151, Korea.
Juwon AhnBundang CHA Medical Center, Department of Neurosurgery, CHA University, Yatap-dong 59, Seongnam 13496, Korea.
Jeongmin SimBundang CHA Medical Center, Department of Neurosurgery, CHA University, Yatap-dong 59, Seongnam 13496, Korea.
Ji-In BangBundang CHA Medical Center, Department of Nuclear Medicine, CHA University, Yatap-dong 59, Seongnam 13496, Korea.ORCID 0000-0003-2962-3642
Jinhyung HeoBundang CHA Medical Center, Department of Pathology, CHA University, Yatap-dong 59, Seongnam 13496, Korea.ORCID 0000-0002-4037-4491
Hyejeong ChoiBundang CHA Medical Center, Department of Radiology, CHA University, Yatap-dong 59, Seongnam 13496, Korea.
Kyunggi ChoBundang CHA Medical Center, Department of Neurosurgery, CHA University, Yatap-dong 59, Seongnam 13496, Korea.
Mihye LeeDepartment of Integrated Biomedical Science, Soonchunhyang Institute of Medi-bio Science (SIMS), Soonchunhyang University, Cheonan 31151, Korea.
Jong-Seok MoonDepartment of Integrated Biomedical Science, Soonchunhyang Institute of Medi-bio Science (SIMS), Soonchunhyang University, Cheonan 31151, Korea.ORCID 0000-0002-2537-7854
Jaejoon LimBundang CHA Medical Center, Department of Neurosurgery, CHA University, Yatap-dong 59, Seongnam 13496, Korea.ORCID 0000-0001-8299-8078
CHA University Bundang Medical Center · KRSoonchunhyang University · KR

Funding

National Research Foundation of Korea NRF-2019M3E5D1A02069071 to J.-S.M.National Research Foundation of Korea NRF-2021R1A2C4002421 to M.L.National Research Foundation of Korea NRF-2021R1C1C1007810 to J.-S.M.National Research Foundation of Korea NRF-2021R1F1A1057801 to J.L.
6 · The paper itself

Abstract

The alteration of the cellular metabolism is a hallmark of glioma. The high glycolytic phenotype is a critical factor in the pathogenesis of high-grade glioma, including glioblastoma multiforme (GBM). GBM has been stratified into three subtypes as the proneural, mesenchymal, and classical subtypes. High glycolytic activity was found in mesenchymal GBM relative to proneural GBM. NADPH oxidase 2 (NOX2) has been linked to cellular metabolism and epithelial-mesenchymal transition (EMT) in tumors. The role of NOX2 in the regulation of the high glycolytic phenotype and the gain of the mesenchymal subtype in glioma remain unclear. Here, our results show that the levels of NOX2 were elevated in patients with GBM. NOX2 induces hexokinase 2 (HK2)-dependent high glycolytic activity in U87MG glioma cells. High levels of NOX2 are correlated with high levels of HK2 and glucose uptake in patients with GBM relative to benign glioma. Moreover, NOX2 increases the expression of mesenchymal-subtype-related genes, including

Indexed as

COL5A1GBMglycolysismesenchymal phenotypeNOX2

Identifiers

PMID35158782
PMCPMC8833670
OpenAlexW4206949100

What OpenQuestion holds

Textmetadata
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.