Evidence map›Paper›PMID 34516556›Full record

ArticlePloS one2021

Cancer-associated IDH mutations induce Glut1 expression and glucose metabolic disorders through a PI3K/Akt/mTORC1-Hif1α axis.

Xun Liu, Kiyoshi Yamaguchi, Kiyoko Takane, Chi Zhu, Makoto Hirata, Yoko Hikiba, Shin Maeda, Yoichi Furukawa, Tsuneo Ikenoue

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
0.9field-weighted citation impact, top 31% 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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Article
  6. Direct targeting of GLUT1 in cancer: A decade of inhibitor discovery and medicinal chemistry insights.Medicinal chemistry research : an international journal for rapid communications on design and mechanisms of action of biologically active agents · 2026
    Review
  7. Review
  8. Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Protein Kinase B (PKB/AKT) Protects IDH-Mutated Glioma from Ferroptosis via Nrf2.Clinical cancer research : an official journal of the American Association for Cancer Research · 2023
    Article
  15. Article
  16. Article
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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

9 authors at 3 institutions in 1 country.

Xun LiuDivision of Clinical Genome Research, Advanced Clinical Research Center, Institute of Medical Science, The University of Tokyo, Minato-ku, Tokyo, Japan.ORCID 0000-0002-2110-5018
Kiyoshi YamaguchiDivision of Clinical Genome Research, Advanced Clinical Research Center, Institute of Medical Science, The University of Tokyo, Minato-ku, Tokyo, Japan.
Kiyoko TakaneDivision of Clinical Genome Research, Advanced Clinical Research Center, Institute of Medical Science, The University of Tokyo, Minato-ku, Tokyo, Japan.
Chi ZhuDivision of Clinical Genome Research, Advanced Clinical Research Center, Institute of Medical Science, The University of Tokyo, Minato-ku, Tokyo, Japan.
Makoto HirataLaboratory of Genome Technology, Institute of Medical Science, University of Tokyo, Minato-ku, Tokyo, Japan.ORCID 0000-0002-9994-9958
Yoko HikibaDepartment of Gastroenterology, Yokohama City University Graduate School of Medicine, Yokohama, Kanagawa Prefecture, Japan.
Shin MaedaDepartment of Gastroenterology, Yokohama City University Graduate School of Medicine, Yokohama, Kanagawa Prefecture, Japan.
Yoichi FurukawaDivision of Clinical Genome Research, Advanced Clinical Research Center, Institute of Medical Science, The University of Tokyo, Minato-ku, Tokyo, Japan.
Tsuneo IkenoueDivision of Clinical Genome Research, Advanced Clinical Research Center, Institute of Medical Science, The University of Tokyo, Minato-ku, Tokyo, Japan.ORCID 0000-0001-8264-2573
The University of Tokyo · JPYokohama City University · JPNational Cancer Center Hospital East · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Isocitrate dehydrogenase 1 and 2 (IDH1/2) mutations and their key effector 2-hydroxyglutarate (2-HG) have been reported to promote oncogenesis in various human cancers. To elucidate molecular mechanism(s) associated with IDH1/2 mutations, we established mouse embryonic fibroblasts (MEF) cells and human colorectal cancer cells stably expressing cancer-associated IDH1R132C or IDH2R172S, and analyzed the change in metabolic characteristics of the these cells. We found that IDH1/2 mutants induced intracellular 2-HG accumulation and inhibited cell proliferation. Expression profile analysis by RNA-seq unveiled that glucose transporter 1 (Glut1) was induced by the IDH1/2 mutants or treatment with 2-HG in the MEF cells. Consistently, glucose uptake and lactate production were increased by the mutants, suggesting the deregulation of glucose metabolism. Furthermore, PI3K/Akt/mTOR pathway and Hif1α expression were involved in the up-regulation of Glut1. Together, these results suggest that Glut1 is a potential target regulated by cancer-associated IDH1/2 mutations.

Indexed as

AnimalsCell ProliferationFibroblastsGene Expression Regulation, NeoplasticGlucoseGlucose Metabolism DisordersGlucose Transporter Type 1GlutaratesGlycolysisHCT116 CellsHumansHypoxia-Inducible Factor 1, alpha SubunitIntracellular SpaceIsocitrate DehydrogenaseLactic AcidMechanistic Target of Rapamycin Complex 1alpha-hydroxyglutarateGlucoseGlucose Transporter Type 1GlutaratesHif1a protein, mouseHypoxia-Inducible Factor 1, alpha SubunitIsocitrate DehydrogenaseLactic AcidMechanistic Target of Rapamycin Complex 1Mutant ProteinsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-akt

Identifiers

PMID34516556
PMCPMC8437293
OpenAlexW3199985847

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.