Evidence map›Paper›PMID 29479058›Full record

ArticleOncogene2018

Targeting UDP-α-D-glucose 6-dehydrogenase inhibits glioblastoma growth and migration.

Olutobi Oyinlade, Shuang Wei, Bachchu Lal, John Laterra, Heng Zhu, C Rory Goodwin, Shuyan Wang, Ding Ma, Jun Wan, Shuli Xia

Abstract read
In one paragraph

Article in Oncogene, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

33 citing papers in PubMed, 45 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. UDP-6-glucose dehydrogenase in hormonally responsive breast cancers.bioRxiv : the preprint server for biology · 2024
    Article
  9. Article
  10. Cancers · 2023
    Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. SP and KLF Transcription Factors in Cancer Metabolism.International journal of molecular sciences · 2022
    Review
  16. Article
  17. Article
  18. Review
  19. Article
  20. 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

10 authors at 4 institutions in 2 countries.

Olutobi OyinladeHugo W. Moser Research Institute at Kennedy Krieger, Baltimore, MD, 21205, USA.
Shuang WeiHugo W. Moser Research Institute at Kennedy Krieger, Baltimore, MD, 21205, USA.
Bachchu LalHugo W. Moser Research Institute at Kennedy Krieger, Baltimore, MD, 21205, USA.ORCID http://orcid.org/0000-0002-5936-0276
John LaterraHugo W. Moser Research Institute at Kennedy Krieger, Baltimore, MD, 21205, USA.
Heng ZhuDepartment of Pharmacology and Molecular Sciences, Johns Hopkins School of Medicine, Baltimore, MD, 21205, USA.
C Rory GoodwinDepartment of Neurosurgery, Duke University Medical Center, Durham, NC, 27710, USA.
Shuyan WangHugo W. Moser Research Institute at Kennedy Krieger, Baltimore, MD, 21205, USA.
Ding MaHugo W. Moser Research Institute at Kennedy Krieger, Baltimore, MD, 21205, USA.
Jun WanDepartment of Medical and Molecular Genetics, Indiana University School of Medicine, Indianapolis, IN, 46202, USA.
Shuli XiaHugo W. Moser Research Institute at Kennedy Krieger, Baltimore, MD, 21205, USA. xia@kennedykrieger.org.
Kennedy Krieger Institute · USDuke Medical Center · USIndiana University School of MedicineJohns Hopkins University · US

Funding

BIOCHEMISTRY, CELLULAR AND MOLECULAR BIOLOGY PROGRAMT32GM007445 · NIGMS · JOHNS HOPKINS UNIVERSITY · PI GREEN, RACHEL · 1985 to 2021
$24.1M
Monospecific monoclonal antibodies against human transcription factorsU54HG006434 · NHGRI · JOHNS HOPKINS UNIVERSITY · PI BLACKSHAW, SETH, ZHU, HENG · 2011 to 2015
$13.8M
Proteome Characterization Center: A Genoproteomics Pipeline for Cance ResearchU24CA160036 · NCI · JOHNS HOPKINS UNIVERSITY · PI CHAN, DANIEL WANYUI, ZHANG, HUI · 2011 to 2016
$10.7M
Chromatin Modifications in GBM-Propagating CellsR01NS096754 · NINDS · HUGO W. MOSER RES INST KENNEDY KRIEGER · PI LATERRA, JOHN J · 2017 to 2021
$2.2M
Methyl-CpG-dependent transcription factor function in human gliomaR01NS091165 · NINDS · HUGO W. MOSER RES INST KENNEDY KRIEGER · PI XIA, SHULI · 2015 to 2019
$1.8M
Brain Cancer Stem Cell Reprogramming by c-MetR01NS073611 · NINDS · HUGO W. MOSER RES INST KENNEDY KRIEGER · PI LATERRA, JOHN J · 2012 to 2016
$1.8M
Suppression of Glioblastoma Stem Cells by Kruppel-Like Factor 9R01NS076759 · NINDS · HUGO W. MOSER RES INST KENNEDY KRIEGER · PI LATERRA, JOHN J · 2011 to 2015
$1.6M
Epigenetics-mediated transcription regulation in mammalsR01GM111514 · NIGMS · JOHNS HOPKINS UNIVERSITY · PI QIAN, JIANG, ZHOU, FENGQUAN · 2014 to 2017
$1.4M
Development of a virion display (VirD) array to profile human GPCR interactionsR33CA186790 · NCI · JOHNS HOPKINS UNIVERSITY · PI DESAI, PRASHANT J, ZHU, HENG · 2015 to 2017
$1.2M
NCI NIH HHS R33 CA186790NCI NIH HHS U24 CA160036NHGRI NIH HHS U54 HG006434NIGMS NIH HHS R01 GM111514NIGMS NIH HHS T32 GM007445NINDS NIH HHS R01 NS073611NINDS NIH HHS R01 NS076759NINDS NIH HHS R01 NS091165NINDS NIH HHS R01 NS096754
6 · The paper itself

Abstract

UDP-glucose 6-dehydrogenase (UGDH) produces UDP-α-D-glucuronic acid, the precursors for glycosaminoglycans (GAGs) and proteoglycans of the extracellular matrix. Elevated GAG formation has been implicated in a variety of human diseases, including glioblastoma (GBM). In our previous study, we found that Krüppel-like factor 4 (KLF4) promotes GBM cell migration by binding to methylated DNA, mainly methylated CpGs (mCpG) and transactivating gene expression. We identified UDGH as one of the downstream targets of KLF4-mCpG binding activity. In this study, we show that KLF4 upregulates UGDH expression in a mCpG-dependent manner, and UGDH is required for KLF4-induced cell migration in vitro. UGDH knockdown decreases GAG abundance in GBM cells, as well as cell proliferation and migration in vitro. In intracranial xenografts, reduced UGDH inhibits tumor growth and migration, accompanied by a decrease in the expression of extracellular matrix proteins such as tenascin C, brevican. Our studies demonstrate a novel DNA methylation-dependent UGDH upregulation by KLF4. Developing UGDH antagonists to decrease the synthesis of extracellular matrix components will be a useful strategy for GBM therapy.

Indexed as

Up-RegulationAnimalsBrain NeoplasmsCell Line, TumorCell MovementCell ProliferationCpG IslandsDNA MethylationEnzyme InhibitorsGene Knockdown TechniquesGlioblastomaGlycosaminoglycansHumansKruppel-Like Factor 4Kruppel-Like Transcription FactorsMiceEnzyme InhibitorsGlycosaminoglycansKLF4 protein, humanKlf4 protein, mouseKruppel-Like Factor 4Kruppel-Like Transcription FactorsProteoglycansUridine Diphosphate Glucose Dehydrogenase

Identifiers

PMID29479058
PMCPMC5957772
OpenAlexW2792075245

What OpenQuestion holds

Textmetadata
LicenceTDM
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.