Cited by 176Cancer, Hypoxia, and MetabolismAmino Acid Enzymes and MetabolismCancer Research and Treatments

Glutamine: pleiotropic roles in tumor growth and stress resistance

Shanware, Naval P., Mullen, Andrew R., DeBerardinis, Ralph J., Abraham, Robert T.·2011·Journal of Molecular Medicine

Abstract

Tumors and tumor cell lines rapidly consume the amino acid glutamine (Gln) and use it to supply metabolic pathways that support cell growth and proliferation. Much of the research regarding the relationship between glutamine metabolism and cancer is based on the premise that this abundant nutrient represents an important driver of tumor cell anabolism. However, Gln's influence in cell biology and cancer extends far beyond its use as a carbon and nitrogen source for the structural components of dividing cells. Gln is truly a multipurpose nutrient, feeding many additional pathways that boost the ability of cells to communicate with each other and to cope with stress by oncogenic signaling and by the tumor microenvironment. A number of recent reports have highlighted these "non-anabolic" functions of Gln metabolism in regulating cell survival, oxidative stress resistance, signal transduction, and autophagy. Here, we review some of these findings and discuss their relevance to tumor biology and the potential for cancer therapy.

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Crossref · 10.1007/s00109-011-0731-9

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  • Aggressive tumor growth requires a restructuring of metabolism to meet the bioenergetic and biosynthetic demands of rapid cell growth and to protect the cells against stresses induced by a harsh microenvironment.

    “One common hypothesis to unify these metabolic pathways is that aggressive tumor growth requires a restructuring of metabolism to meet the bioenergetic and biosynthetic demands of rapid cell growth and to protect the cells against stresses induced by a harsh microenvironment (Deberardinis et al., 2008; Semenza, 2010; Shanware et al., 2011).”

    From Cellular Metabolism and Disease: What Do Metabolic Outliers Teach Us? (2012) · cites this paper as Shanware et al., 2011

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Authors
Shanware, N. P., Mullen, A. R., DeBerardinis, R. J., & Abraham, R. T.
Affiliations
  • Pfizer (United States) (US)
  • The University of Texas Southwestern Medical Center (US)
Corresponding author
Abraham, Robert T.
Venue
Journal of Molecular Medicine
Published
2011-02-08
Volume
89
Issue
3
Pages
229-236
ISSN
  • 0946-2716 (ISSN-L)
  • 1432-1440
OpenAlex
W2146867504
Cited by
176
References
43
Citations by year
2026: 2 · 2025: 3 · 2024: 12 · 2023: 8 · 2022: 18 · 2021: 7 · 2020: 14 · 2019: 11 · 2018: 14 · 2017: 11 · 2016: 9 · 2015: 17 · 2014: 19 · 2013: 12 · 2012: 10
FWCI
1.16
Type
journal article
Language
en
Open access
closed
Locations
  • Journal of Molecular Medicine (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Amino Acid Enzymes and Metabolism
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Biotechnology › Cancer Research and Treatments
Keywords
glutamine metabolism, tumor growth, stress tolerance, oxidative stress resistance, tumor microenvironment, oncogenic signaling, cell survival, signal transduction, autophagy, cancer therapy, glutamine deprivation
MeSH terms
Autophagy, Glutamine, Models, Biological, Neoplasms, Oxidative Stress

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