Evidence map›Paper›PMID 25605240›Full record

ArticleOncotarget2015

Hypoxia induces a lipogenic cancer cell phenotype via HIF1α-dependent and -independent pathways.

Alessandro Valli, Miguel Rodriguez, Loukas Moutsianas, Roman Fischer, Vita Fedele, Hong-Lei Huang, Ruud Van Stiphout, Dylan Jones, Michael Mccarthy, Maria Vinaxia and 8 more

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
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

49 citing papers in PubMed, 78 citations in OpenAlex.

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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

18 authors at 5 institutions in 3 countries.

Alessandro ValliWeatherall Institute of Molecular Medicine, University of Oxford, Oxford, UK.
Miguel RodriguezCentre for Omic Sciences, Rovira i Virgili University, Reus, Spain.
Loukas MoutsianasThe Wellcome Trust Centre for Human Genetics, Nuffield Department of Medicine, Oxford, UK.
Roman FischerTarget Discovery Institute, Nuffield Department of Medicine, University of Oxford, Oxford, UK.
Vita FedeleTarget Discovery Institute, Nuffield Department of Medicine, University of Oxford, Oxford, UK.
Hong-Lei HuangTarget Discovery Institute, Nuffield Department of Medicine, University of Oxford, Oxford, UK.
Ruud Van StiphoutWeatherall Institute of Molecular Medicine, University of Oxford, Oxford, UK.
Dylan JonesWeatherall Institute of Molecular Medicine, University of Oxford, Oxford, UK.
Michael MccarthyTarget Discovery Institute, Nuffield Department of Medicine, University of Oxford, Oxford, UK.
Maria VinaxiaCentre for Omic Sciences, Rovira i Virgili University, Reus, Spain.
Kaori IgarashiInstitute for Advanced Biosciences, Keio University, Tsuruoka, Yamagata, Japan.
Maya SatoInstitute for Advanced Biosciences, Keio University, Tsuruoka, Yamagata, Japan.
Tomoyoshi SogaInstitute for Advanced Biosciences, Keio University, Tsuruoka, Yamagata, Japan.
Francesca BuffaWeatherall Institute of Molecular Medicine, University of Oxford, Oxford, UK.
James MccullaghMass Spectrometry Research Facility CRL, Department of Chemistry, University of Oxford, Oxford, UK.
Oscar YanesCentre for Omic Sciences, Rovira i Virgili University, Reus, Spain.
Adrian HarrisWeatherall Institute of Molecular Medicine, University of Oxford, Oxford, UK.
Benedikt KesslerTarget Discovery Institute, Nuffield Department of Medicine, University of Oxford, Oxford, UK.
University of Oxford · GBKeio University · JPUniversidad Rovira i Virgili · ESMRC Weatherall Institute of Molecular Medicine · GBCentre for Human Genetics · GB

Funding

Cancer Research UK 11359Cancer Research UK 16466Cancer Research UK 18974
6 · The paper itself

Abstract

The biochemistry of cancer cells diverges significantly from normal cells as a result of a comprehensive reprogramming of metabolic pathways. A major factor influencing cancer metabolism is hypoxia, which is mediated by HIF1α and HIF2α. HIF1α represents one of the principal regulators of metabolism and energetic balance in cancer cells through its regulation of glycolysis, glycogen synthesis, Krebs cycle and the pentose phosphate shunt. However, less is known about the role of HIF1α in modulating lipid metabolism. Lipids serve cancer cells to provide molecules acting as oncogenic signals, energetic reserve, precursors for new membrane synthesis and to balance redox biological reactions. To study the role of HIF1α in these processes, we used HCT116 colorectal cancer cells expressing endogenous HIF1α and cells in which the hif1α gene was deleted to characterize HIF1α-dependent and independent effects on hypoxia regulated lipid metabolites. Untargeted metabolomics integrated with proteomics revealed that hypoxia induced many changes in lipids metabolites. Enzymatic steps in fatty acid synthesis and the Kennedy pathway were modified in a HIF1α-dependent fashion. Palmitate, stearate, PLD3 and PAFC16 were regulated in a HIF-independent manner. Our results demonstrate the impact of hypoxia on lipid metabolites, of which a distinct subset is regulated by HIF1α.

Indexed as

Lipid MetabolismSignal TransductionAcetyl-CoA C-AcyltransferaseAcetyl-CoA CarboxylaseAgedBasic Helix-Loop-Helix ProteinsBlotting, WesternCell HypoxiaCell Line, TumorColorectal NeoplasmsEndothelial PAS Domain-Containing Protein 1Fatty AcidsFemaleGenomicsHCT116 CellsHumansACAA1 protein, humanACACA protein, humanAcetyl-CoA C-AcyltransferaseAcetyl-CoA CarboxylaseBasic Helix-Loop-Helix ProteinsEndothelial PAS Domain-Containing Protein 1Fatty AcidsHypoxia-Inducible Factor 1, alpha SubunitLipidsPlatelet Activating Factor

Identifiers

PMID25605240
PMCPMC4385826
OpenAlexW1884217239

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.