Cited by 148Cancer, Hypoxia, and MetabolismAutophagy in Disease and TherapyAmino Acid Enzymes and Metabolism

Glutaminolysis and autophagy in cancer

Open access
Villar, Victor H, Merhi, Faten, Djavaheri-Mergny, Mojgan, Durán, Raúl V·2015·Autophagy

Abstract

The remarkable metabolic differences between cancer cells and normal cells result in the potential for targeted cancer therapy. The upregulation of glutaminolysis provides energetic advantages to cancer cells. The recently described link between glutaminolysis and autophagy, mediated by MTORC1, may constitute an attractive target for therapeutic strategies. A combination of therapies targeting simultane-ously cell signaling, cancer metabolism, and autophagy can solve therapy resistance and tumor relapse problems, commonly observed in patients treated with most of the current targeted therapies. In this review we summarize the mechanistic link between glutaminolysis and autophagy, and discuss the impacts of these processes on cancer progression and the potential for therapeutic intervention.

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Crossref · 10.1080/15548627.2015.1053680

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  • Enhanced glutaminolysis might contribute to cancer initiation and progression by stimulating cell growth via mTORC1 and aerobic glycolysis while inhibiting autophagy and the DNA damage response.

    “Therefore, enhanced glutaminolysis might eventually contribute to the initiation and progression of cancer by stimulating cell growth via the mTORC1 pathway and enhancing aerobic glycolysis while disrupting the proper elimination of misfolded proteins, damaged DNA and organelles through the inhibition of autophagy and the DNA damage response166.”

    From Glutamine reliance in cell metabolism (2020) · cites this paper as [166]

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Authors
Villar, V. H., Merhi, F., Djavaheri-Mergny, M., & Durán, R. V.
Affiliations
  • Université de Bordeaux (FR)
  • INSERM U916 VINCO; Institut Bergonié; Bordeaux, France
Corresponding author
Durán, Raúl V
Venue
Autophagy
Published
2015-08-03
Volume
11
Issue
8
Pages
1198-1208
ISSN
  • 1554-8627 (ISSN-L)
  • 1554-8635
OpenAlex
W1768966319
Cited by
143
References
145
Citations by year
2026: 6 · 2025: 15 · 2024: 14 · 2023: 9 · 2022: 18 · 2021: 18 · 2020: 18 · 2019: 12 · 2018: 15 · 2017: 12 · 2016: 5 · 2015: 1
FWCI
1.07
Type
journal article
Language
en
Open access
Locations
  • Autophagy (publishedVersion)
  • Europe PMC (PubMed Central) (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
  • HAL (submittedVersion)
Funders
  • Institut National de la Santé et de la Recherche Médicale
  • Fondation ARC pour la Recherche sur le Cancer
  • Ligue Contre le Cancer
  • Institut National Du Cancer
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
  • Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Amino Acid Enzymes and Metabolism
Keywords
glutaminolysis, cancer metabolism, mTORC1 signaling, cancer cell energy metabolism, targeted cancer therapy, treatment resistance, tumor recurrence, tumor progression
MeSH terms
Mechanistic Target of Rapamycin Complex 1, Animals, Autophagy, Cell Transformation, Neoplastic, Glutamine, Humans, Ketoglutaric Acids, Neoplasm Recurrence, Local, Neoplasms, Signal Transduction, Gene Expression Regulation, Neoplastic, Reactive Oxygen Species, Drug Resistance, Neoplasm, Multiprotein Complexes, Cell Proliferation, TOR Serine-Threonine Kinases

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