Q's next: The diverse functions of glutamine in metabolism, cell biology and cancer

By Ralph J. Deberardinis, Tzuling Cheng. Oncogene, 2009

1,316 citations recorded by the source corpus.

Several decades of research have sought to characterize tumor cell metabolism in the hope that tumor-specific activities can be exploited to treat cancer. Having originated from Warburg's seminal observation of aerobic glycolysis in tumor cells, most of this attention has focused on glucose metabolism. However, since the 1950s cancer biologists have also recognized the importance of glutamine (Q) as a tumor nutrient. Glutamine contributes to essentially every core metabolic task of proliferating tumor cells: it participates in bioenergetics, supports cell defenses against oxidative stress and complements glucose metabolism in the production of macromolecules. The interest in glutamine metabolism has been heightened further by the recent findings that c-myc controls glutamine uptake and degradation, and that glutamine itself exerts influence over a number of signaling pathways that contribute to tumor growth. These observations are stimulating a renewed effort to understand the regulation of glutamine metabolism in tumors and to develop strategies to target glutamine metabolism in cancer. In this study we review the protean roles of glutamine in cancer, both in the direct support of tumor growth and in mediating some of the complex effects on whole-body metabolism that are characteristic of tumor progression.

Subfields: Biochemistry, Cancer Research, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/ce969ce78e5f36fbc416f7e0e84ffaffb9a3fc77

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Citations in the corpus

The Metabolic Profile of Tumors Depends on both the Responsible Genetic Lesion and Tissue Type (2012, background): “This suggests that other pathways of glutamine metabolism may provide the opportunity for additional synthetic lethal interactions with the overexpression of MYC (DeBerardinis and Cheng, 2010; Mates et al., 2006).”
ROS homeostasis and metabolism: a dangerous liason in cancer cells (2016, background): “To replenish the TCA cycle substrates and fuel their uncontrolled growth, cancer cells utilize specific mechanisms of anaplerosis on the basis of the oxidation of glutamine to α-ketoglutarate and its conversion to oxaloacetate.(136) As a consequence of oxidative metabolism, physiological amounts of ”
Lipid metabolism reprogramming and its potential targets in cancer (2018, background): “Glutamine transporters, such as SLC1A5 (also known as ASCT2), are up-regulated in various cancers [65, 66].”
MYC, Metabolism, and Cancer. (2015, background): “Later studies indicated that glutamine, the most abundant circulating free amino acid in human plasma, can act as a source of carbon and nitrogen in cancer cells (112).”
Cancer as a metabolic disease (2010, background): “Although dietary energy restriction and anti-glycolytic cancer drugs will have therapeutic efficacy against many tumors that depend largely on glycolysis and glucose for growth, these therapeutic approaches could be less effective against those tumor cells that depend more heavily on glutamine than ”
MYC, metabolism, cell growth, and tumorigenesis. (2013, background): “In addition, MYC was found to induce the expression of other genes involved in glutamine metabolism, such as glutamine transporters (ASCT2 [SLC1A5] and SLC7A5).”
Cancer Cell Metabolism: One Hallmark, Many Faces (2012, background): “Instead, the importance of glutamine as an additionally critical nutrient in broadly fueling proliferation has also become better understood and appreciated in recent years (18).”
Energy metabolism of cancer: Glycolysis versus oxidative phosphorylation (Review). (2012, background): “Many intermediates from glycolysis, truncated TCA and glutaminolysis are used in cell biosynthesis during the cancer cell metabolic switch to glycolysis by Ras and Myc (40,57).”
Glutamine Addiction: A New Therapeutic Target in Cancer (2010, background): “In some tumors, this seemingly wasteful metabolism of glucose is mirrored by a similarly inefficient metabolism of glutamine [10,11].”
Distinct Regulation of Th17 and Th1 Cell Differentiation by Glutaminase-Dependent Metabolism (2018, background): “Glutamine is a conditionally essential amino acid in rapidly proliferating cells (Curthoys and Watford, 1995) and a potential target in cancer treatment (DeBerardinis and Cheng, 2010; Cheng et al., 2011; Wise and Thompson, 2010).”
Glutamine and cancer: cell biology, physiology, and clinical opportunities. (2013, neutral): “Glutamine metabolism has been reviewed extensively and is briefly outlined here (4, 5).”