Evidence map›Paper›PMID 24465898›Full record

ArticlePloS one2014

The role of factor inhibiting HIF (FIH-1) in inhibiting HIF-1 transcriptional activity in glioblastoma multiforme.

Enfeng Wang, Chunyang Zhang, Navatha Polavaram, Fengming Liu, Gang Wu, Mark A Schroeder, Julie S Lau, Debabrata Mukhopadhyay, Shi-Wen Jiang, Brian Patrick O'Neill and 2 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 19% 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

35 citing papers in PubMed, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.

  1. Pooled it
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  6. Review
  7. Treatment with the vascular endothelial growth factor-A antibody, bevacizumab, has sex-specific effects in a rat model of mild traumatic brain injury.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2024
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  17. Regulation of Transactivation at C-TAD Domain of HIF-1Oxidative medicine and cellular longevity · 2022
    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

12 authors at 5 institutions in 2 countries.

Enfeng WangDepartment of Biochemistry and Molecular Biology, Mayo Clinic Cancer Center, Rochester, Minnesota, United States of America.
Chunyang ZhangDepartment of Neuro-Surgery, the First Affiliated Hospital of Baotou Medical College, Baotou, China.
Navatha PolavaramDepartment of Biochemistry and Molecular Biology and Eppley Cancer Center, University of Nebraska Medical Center, Omaha, Nebraska, United States of America.
Fengming LiuDepartment of Research and Development, Guangxi Medicinal Botanical Institute, Nanning, Guangxi, China.
Gang WuDepartment of Biochemistry and Molecular Biology, Mayo Clinic Cancer Center, Rochester, Minnesota, United States of America.
Mark A SchroederDepartment of Radiation Oncology, Mayo Clinic Cancer Center, Rochester, Minnesota, United States of America.
Julie S LauDepartment of Biochemistry and Molecular Biology, Mayo Clinic Cancer Center, Rochester, Minnesota, United States of America.
Debabrata MukhopadhyayDepartment of Biochemistry and Molecular Biology, Mayo Clinic Cancer Center, Rochester, Minnesota, United States of America.
Shi-Wen JiangDepartment of Biomedical Science, Mercer University School of Medicine, Savannah, Georgia, United States of America ; Department of Obstetrics and Gynecology, Memorial Health Hospital, Savannah, Georgia, United States of America.
Brian Patrick O'NeillDepartment of Biochemistry and Molecular Biology, Mayo Clinic Cancer Center, Rochester, Minnesota, United States of America.
Kaustubh DattaDepartment of Biochemistry and Molecular Biology and Eppley Cancer Center, University of Nebraska Medical Center, Omaha, Nebraska, United States of America.
Jinping LiDepartment of Biomedical Science, Mercer University School of Medicine, Savannah, Georgia, United States of America ; Department of Obstetrics and Gynecology, Memorial Health Hospital, Savannah, Georgia, United States of America.
Mayo Clinic · USMercer University Health Sciences Center · USUniversity of Nebraska Medical Center · USBaotou Medical College · CNGuangxi Medicinal Botanical Garden · CN

Funding

Women's Cancer ProgramP30CA015083 · NCI · MAYO CLINIC ROCHESTER · PI Felicity Enders · 1985 to 2026
$151.3M
Targeted MV-CEA as a Potent Antitumor Agent against GBMP50CA108961 · NCI · MAYO CLINIC ROCHESTER · PI O'NEILL, BRIAN PATRICK · 2004 to 2015
$22.5M
The role of VEGF-C in resisting stress in prostate cancerR01CA140432 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI DATTA, KAUSTUBH · 2010 to 2014
$1.5M
NCI NIH HHS P30 CA015083NCI NIH HHS P50 CA108961NCI NIH HHS P50CA108961NCI NIH HHS R01 CA140432
6 · The paper itself

Abstract

Glioblastoma multiforme (GBM) accounts for about 38% of primary brain tumors in the United States. GBM is characterized by extensive angiogenesis induced by vascular growth factors and cytokines. The transcription of these growth factors and cytokines is regulated by the Hypoxia-Inducible-Factor-1(HIF-1), which is a key regulator mediating the cellular response to hypoxia. It is known that Factor Inhibiting HIF-1, or FIH-1, is also involved in the cellular response to hypoxia and has the capability to physically interact with HIF-1 and block its transcriptional activity under normoxic conditions. Delineation of the regulatory role of FIH-1 will help us to better understand the molecular mechanism responsible for tumor growth and progression and may lead to the design of new therapies targeting cellular pathways in response to hypoxia. Previous studies have shown that the chromosomal region of 10q24 containing the FIH-1 gene is often deleted in GBM, suggesting a role for the FIH-1 in GBM tumorigenesis and progression. In the current study, we found that FIH-1 is able to inhibit HIF-mediated transcription of GLUT1 and VEGF-A, even under hypoxic conditions in human glioblastoma cells. FIH-1 has been found to be more potent in inhibiting HIF function than PTEN. This observation points to the possibility that deletion of 10q23-24 and loss or decreased expression of FIH-1 gene may lead to a constitutive activation of HIF-1 activity, an alteration of HIF-1 targets such as GLUT-1 and VEGF-A, and may contribute to the survival of cancer cells in hypoxia and the development of hypervascularization observed in GBM. Therefore FIH-1 can be potential therapeutic target for the treatment of GBM patients with poor prognosis.

Indexed as

Gene Expression Regulation, NeoplasticTranscription, GeneticAnimalsBrain NeoplasmsCell HypoxiaCell Line, TumorE1A-Associated p300 ProteinGlioblastomaGlucose Transporter Type 1HumansHypoxia-Inducible Factor 1, alpha SubunitMiceMice, NudeMixed Function OxygenasesNeoplasm TransplantationRepressor ProteinsE1A-Associated p300 ProteinEP300 protein, humanGlucose Transporter Type 1HIF1AN protein, humanHIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitMixed Function OxygenasesRepressor ProteinsSLC2A1 protein, humanVascular Endothelial Growth Factor AVEGFA protein, human

Identifiers

PMID24465898
PMCPMC3900478
OpenAlexW1979561126

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.