Evidence map›Paper›PMID 31890203›Full record

ArticleCancer & metabolism2019

HIF1/2-exerted control over glycolytic gene expression is not functionally relevant for glycolysis in human leukemic stem/progenitor cells.

Albertus T J Wierenga, Alan Cunningham, Ayşegül Erdem, Nuria Vilaplana Lopera, Annet Z Brouwers-Vos, Maurien Pruis, André B Mulder, Ulrich L Günther, Joost H A Martens, Edo Vellenga and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cancer & metabolism, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
1.7field-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

36 citing papers in PubMed, 44 citations in OpenAlex.

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  15. Hypoxia induces a glycolytic complex in intestinal epithelial cells independent of HIF-1-driven glycolytic gene expression.Proceedings of the National Academy of Sciences of the United States of America · 2023
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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

11 authors at 3 institutions in 2 countries.

Albertus T J WierengaDepartment of Experimental Hematology, University Medical Center Groningen, University of Groningen, Hanzeplein 1, Groningen, 9700RB The Netherlands.
Alan Cunningham *Department of Experimental Hematology, University Medical Center Groningen, University of Groningen, Hanzeplein 1, Groningen, 9700RB The Netherlands.
Ayşegül Erdem *Department of Experimental Hematology, University Medical Center Groningen, University of Groningen, Hanzeplein 1, Groningen, 9700RB The Netherlands.
Nuria Vilaplana Lopera *3Institute of Cancer and Genomic Sciences, University of Birmingham, Birmingham, UK.
Annet Z Brouwers-VosDepartment of Experimental Hematology, University Medical Center Groningen, University of Groningen, Hanzeplein 1, Groningen, 9700RB The Netherlands.
Maurien PruisDepartment of Experimental Hematology, University Medical Center Groningen, University of Groningen, Hanzeplein 1, Groningen, 9700RB The Netherlands.
André B MulderDepartment of Laboratory Medicine, University Medical Center Groningen, University of Groningen, Hanzeplein 1, 9700RB Groningen, The Netherlands.
Ulrich L Günther3Institute of Cancer and Genomic Sciences, University of Birmingham, Birmingham, UK.
Joost H A Martens4Department of Molecular Biology, Radboud Institute for Molecular Life Sciences (RIMLS), Nijmegen, The Netherlands.
Edo VellengaDepartment of Experimental Hematology, University Medical Center Groningen, University of Groningen, Hanzeplein 1, Groningen, 9700RB The Netherlands.
Jan Jacob SchuringaDepartment of Experimental Hematology, University Medical Center Groningen, University of Groningen, Hanzeplein 1, Groningen, 9700RB The Netherlands.ORCID 0000-0001-8452-8555
University Medical Center Groningen · NLCancer Research UK Clinical Trials Unit · GBRadboud University Nijmegen · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHypoxia-inducible factors (HIF)1 and 2 are transcription factors that regulate the homeostatic response to low oxygen conditions. Since data related to the importance of HIF1 and 2 in hematopoietic stem and progenitors is conflicting, we investigated the chromatin binding profiles of HIF1 and HIF2 and linked that to transcriptional networks and the cellular metabolic state.

methodsGenome-wide ChIPseq and ChIP-PCR experiments were performed to identify HIF1 and HIF2 binding sites in human acute myeloid leukemia (AML) cells and healthy CD34

resultsGenome-wide ChIP-seq and transcriptome studies revealed that overlapping HIF1- and HIF2-controlled loci were highly enriched for various processes including metabolism, particularly glucose metabolism, but also for chromatin organization, cellular response to stress and G protein-coupled receptor signaling. ChIP-qPCR validation studies confirmed that glycolysis-related genes but not genes related to the TCA cycle or glutaminolysis were controlled by both HIF1 and HIF2 in leukemic cell lines and primary AMLs, while in healthy human CD34

conclusionThese data indicate that, while HIFs exert control over glycolysis but not OxPHOS gene expression in human leukemic cells, this is not critically important for their metabolic state. In contrast, inhibition of BCR-ABL did impact on glucose consumption and lactate production regardless of the presence of HIFs. These data indicate that oncogene-mediated control over glycolysis can occur independently of hypoxic signaling modules.

Indexed as

Acute myeloid leukemia (AML)BCR-ABLGlycolysisHuman hematopoietic stem cellsHypoxiaHypoxia induced factors (HIFs)

Identifiers

PMID31890203
PMCPMC6935105
OpenAlexW2997868886

What OpenQuestion holds

Textmetadata
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.