Evidence map›Paper›PMID 33723393›Full record

ArticleBritish journal of cancer2021

Autophagy mediated lipid catabolism facilitates glioma progression to overcome bioenergetic crisis.

Chenran Wang, Michael A Haas, Syn Kok Yeo, Ritama Paul, Fuchun Yang, Subrahmanya Vallabhapurapu, Xiaoyang Qi, David R Plas, Jun-Lin Guan

Open access · bronzeAbstract read
In one paragraph

Article in British journal of cancer, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

16 citing papers in PubMed, 16 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Nanovaccines with ferroptosis, necroptosis and STING-activation for synergistic immunotherapy.Journal of experimental & clinical cancer research : CR · 2026
    Article
  6. Article
  7. Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. Targeting fatty acid metabolism in glioblastoma.The Journal of clinical investigation · 2023
    Review
  13. Article
  14. Review
  15. Review
  16. Review
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 2 institutions in 1 country.

Chenran Wang *Department of Cancer Biology, University of Cincinnati College of Medicine, Cincinnati, OH, USA. wang2cr@ucmail.uc.edu.ORCID http://orcid.org/0000-0003-4181-2729
Michael A Haas *Department of Cancer Biology, University of Cincinnati College of Medicine, Cincinnati, OH, USA.
Syn Kok YeoDepartment of Cancer Biology, University of Cincinnati College of Medicine, Cincinnati, OH, USA.
Ritama PaulDepartment of Cancer Biology, University of Cincinnati College of Medicine, Cincinnati, OH, USA.
Fuchun YangDepartment of Cancer Biology, University of Cincinnati College of Medicine, Cincinnati, OH, USA.
Subrahmanya VallabhapurapuDivision of Hematology/Oncology, Department of Internal Medicine, University of Cincinnati College of Medicine, Cincinnati, OH, USA.
Xiaoyang QiDivision of Hematology/Oncology, Department of Internal Medicine, University of Cincinnati College of Medicine, Cincinnati, OH, USA.
David R PlasDepartment of Cancer Biology, University of Cincinnati College of Medicine, Cincinnati, OH, USA.
Jun-Lin GuanDepartment of Cancer Biology, University of Cincinnati College of Medicine, Cincinnati, OH, USA.
University of Cincinnati Medical Center · USUniversity of Cincinnati · US

Funding

Regulation of Neural Stem Cells and Neurogenesis by Autophagy GenesR01NS094144 · NINDS · UNIVERSITY OF CINCINNATI · PI GUAN, JUN-LIN · 2015 to 2024
$3.6M
Mechanisms of FIP200 regulation of breast cancer through its autophagy and non-autophagy functionsR01CA211066 · NCI · UNIVERSITY OF CINCINNATI · PI JUN-LIN GUAN · 2017 to 2026
$3.4M
Co-targeting S6 and TAM kinases in PTEN-deficient glioblastomaR01CA239657 · NCI · UNIVERSITY OF CINCINNATI · PI PLAS, DAVID R · 2020 to 2024
$2.1M
Regulation of Lipid Catabolism by Autophagy in Neural Stem Cell of Tuberous Sclerosis ComplexR01NS103981 · NINDS · UNIVERSITY OF CINCINNATI · PI WANG, CHENRAN · 2018 to 2022
$1.8M
NCI NIH HHS R01 CA211066NCI NIH HHS R01 CA239657NINDS NIH HHS R01 NS094144NINDS NIH HHS R01 NS103981U.S. Department of Health & Human Services | NIH | National Institute of Neurological Disorders and Stroke (NINDS) NS094144U.S. Department of Health & Human Services | NIH | National Institute of Neurological Disorders and Stroke (NINDS) NS103981U.S. Department of Health & Human Services | NIH | NCI | Division of Cancer Epidemiology and Genetics, National Cancer Institute (National Cancer Institute Division of Cancer Epidemiology and Genetics) CA211066
6 · The paper itself

Abstract

backgroundActivation of mTORC1 plays a significant role in cancer development and progression. However, the metabolic mechanisms to sustain mTORC1 activation of cancer cells within stressed environments are still under-appreciated. We recently revealed high autophagy activity in tumour cells with mTORC1 hyper-activation. Nevertheless, the functions and mechanisms of autophagy in regulating mTORC1 in glioma are not studied.

methodsUsing glioma patient database and human glioma cells, we assessed the mechanisms and function of selective autophagy to sustain mTORC1 hyper-activation in glioma.

resultsWe revealed a strong association of altered mRNA levels in mTORC1 upstream and downstream genes with prognosis of glioma patients. Our results indicated that autophagy-mediated lipid catabolism was essential to sustain mTORC1 activity in glioma cells under energy stresses. We found that autophagy inhibitors or fatty acid oxidation (FAO) inhibitors in combination with 2-Deoxy-D-glucose (2DG) decreased energy production and survival of glioma cells in vitro. Consistently, inhibition of autophagy or FAO inhibitors with 2DG effectively suppressed the progression of xenografted glioma with hyper-activated mTORC1.

conclusionsThis study established an autophagy/lipid degradation/FAO/ATP generation pathway, which might be used in brain cancer cells under energy stresses to maintain high mTORC1 signalling for tumour progression.

Indexed as

Lipid MetabolismAnimalsApoptosisAutophagyBrain NeoplasmsCell Line, TumorDisease ProgressionEnergy MetabolismGene Expression Regulation, NeoplasticGliomaHEK293 CellsHumansMechanistic Target of Rapamycin Complex 1MiceMice, NudeSignal TransductionMechanistic Target of Rapamycin Complex 1

Identifiers

PMID33723393
PMCPMC8110959
OpenAlexW3136328008

What OpenQuestion holds

Textmetadata
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.