Nitrogen anabolism underlies the importance of glutaminolysis in proliferating cells

Meng, Meng; Chen, Shuyang; Lao, Taotao; Liang, Dongming; Sang, Nianli

doi:10.4161/cc.9.19.13139

Cited by 75 publications

(88 citation statements)

References 53 publications

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“…17 Other authors have described the importance of glutaminolysis and have suggested that the Warburg effect may be a metabolic consequence secondary to nitrogen anabolism (glutaminolysis). 20 Therefore, Dang et al have concluded that glucose metabolism (glycolysis) is insufficient to sustain a growing and dividing cancer cell. The Warburg effect requires glutamine for both redox balance and lipid synthesis.…”

Section: Role Of Hif1 In Ph Regulationmentioning

confidence: 99%

The real face of HIF1α in the tumor process

et al. 2012

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Section: Role Of Hif1 In Ph Regulationmentioning

confidence: 99%

The real face of HIF1α in the tumor process

et al. 2012

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“…Ammonia-induced autophagy protects cells from apoptosis induced by tumor necrosis factor-a and limits cell proliferation under metabolic stress . Cell death induced by long-term culture in glutamine-free medium is also rescued by low concentrations of ammonia (Meng et al, 2010). As these autophagy-promoting concentrations of ammonia are also found in tumor interstitial fluids, ammonia may act as a diffusible autophagy-inducing signal that protects tumor cells located in poorly vascularized regions from metabolic stress .…”

Section: Influence Of Metabolic Reprogramming On Tumor Autophagic Actmentioning

confidence: 98%

The autophagy conundrum in cancer: influence of tumorigenic metabolic reprogramming

Eng

Abraham

2011

Oncogene

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Tumorigenesis is often accompanied by metabolic changes that favor rapid energy production and increased biosynthetic capabilities. These metabolic adaptations promote the survival and proliferation of tumor cells, and in conjunction with the hypoxic and metabolically challenged tumor microenvironment, influence autophagic activity. Autophagy is a catabolic process that allows cellular macromolecules to be broken down and re-utilized as metabolic precursors. Stimulation of autophagy promotes the survival of tumor cells under stressful metabolic and environmental conditions, and counters the potentially deleterious effects of mitochondrial dysfunction and the ROS that these organelles generate. However, inhibition of autophagy has also been reported to fuel tumorigenesis. In spite of the advances in our understanding of the relationship between autophagy and tumorigenesis, it remains unclear whether the therapeutic approaches targeting autophagy should aim to increase or decrease autophagic flux in tumor tissues in human patients. Here, we review how metabolic reprogramming influences autophagic activity in tumors, and discuss how inhibition of autophagy might be exploited to target tumor cells that show altered metabolism.

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“…Early observations showed that ammonia has been linked to the regulation of metabolic processes, such as long-term survival and proliferation of hepatic 3B when glutamine is depleted [145]. However, the idea that ammonia generated during glutaminolysis could presumably modulate macromolecule turnover by autophagy activity boosted the interest in studying ammoniagenesis and cancer metabolic rewiring.…”

Section: Depot For Ammonia and Autophagymentioning

confidence: 99%

Glutamine at focus: versatile roles in cancer

2015

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Your article is protected by copyright and all rights are held exclusively by International Society of Oncology and BioMarkers (ISOBM).Abstract During the past decade, a heightened understanding of metabolic pathways in cancer has significantly increased. It is recognized that many tumor cells are genetically programmed and have involved an abnormal metabolic state. Interestingly, this increased metabolic autonomy generates dependence on various nutrients such as glucose and glutamine. Both of these components participate in various facets of metabolic activity that allow for energy production, synthesis of biomass, antioxidant defense, and the regulation of cell signaling. Here, we outline the emerging data on glutamine metabolism and address the molecular mechanisms underlying glutamine-induced cell survival. We also discuss novel therapeutic strategies to exploit glutamine addiction of certain cancer cell lines.

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Nitrogen anabolism underlies the importance of glutaminolysis in proliferating cells

Cited by 75 publications

References 53 publications

The real face of HIF1α in the tumor process

The real face of HIF1α in the tumor process

The autophagy conundrum in cancer: influence of tumorigenic metabolic reprogramming

Glutamine at focus: versatile roles in cancer

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