Relevance of glutamine metabolism to tumor cell growth

Medina, Miguel Ángel; Sánchez‐Jiménez, Francisca; Márquez, Javier; Quesada, Ana R.; Castro, Ignacio Núñez de

doi:10.1007/bf00230880

Cited by 170 publications

(126 citation statements)

References 104 publications

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“…Although, ATA1 is primarily expressed in neurons, and not in normal liver (7), our results demonstrate that its expression is significantly elevated both in HCC tissues and HCC cell lines. In this regard, it is noteworthy that since tumors use glutamine as a primary metabolic fuel and nitrogen source (28,29), a marked depletion of plasma glutamine occurs in patients with liver cancer (30). Hence, such an ectopic activation of ATA1 may be a compensatory amino acid uptake mechanism that confers a survival advantage in HCC cells.…”

Section: Discussionmentioning

confidence: 99%

Activation of a system A amino acid transporter, ATA1/SLC38A1, in human hepatocellular carcinoma and preneoplastic liver tissues

Kondoh

Imazeki²,

Arai³

et al. 2007

Int J Oncol

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Abstract. The expression of amino acid transporter (AT) mRNAs including A system (ATA1/SNAT1/SLC38A1, ATA2/ SNAT2/SLC38A2 and ATA3/SNAT3/SLC38A4), L system (LAT1/SLC7A5 and LAT2/SLC7A8), and y + (CAT2/SLC7A2) genes, were compared among hepatocellular carcinoma (HCC) and non-cancerous liver cells. Among them the ATA1 mRNA expression was significantly elevated in all HCC cell lines (HepG2, HLF, HuH7 and JHH4) examined compared with normal liver tissue. We further discovered that the expression of ATA1 mRNA was significantly activated in HCC tissues and also elevated in pre-malignant cirrhotic livers from HCC patients, compared with normal livers from non-HCC patients. The ATA1 protein was extensively accumulated in the cytoplasm of pre-malignant liver and most HCCs, while being weak or undetectably low in normal liver tissues. SiRNAmediated suppression of endogenous ATA1 lowered the viability of HepG2 cells. Thus, the activation of ATA1 confers growth and survival advantages in pre-malignant and malignant liver lesions.

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Section: Discussionmentioning

confidence: 99%

Activation of a system A amino acid transporter, ATA1/SLC38A1, in human hepatocellular carcinoma and preneoplastic liver tissues

Kondoh

Imazeki²,

Arai³

et al. 2007

Int J Oncol

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“…Glutamine synthetase catalyzes the formation of glutamine from glutamate using ammo nium ions and AlT. It was shown that, in rapidly growing hepatoma cells, the activity of glutamine synthetase was decreased (36). The paradox that glutamine synthetase activity is decreased in tumor cells and that large amounts of glutamine are required for tumor cell growth has not yet been resolved.…”

Section: Discussionmentioning

confidence: 99%

Identification of genes differentially expressed in normal lung and non-small cell lung carcinoma tissue

Schraml

Shipman²,

Colombi³

et al. 1995

Lung Cancer

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Using a magnet-assisted subtraction technique, 17 complementary DNA (eDNA) clones were isOlatedthat were expressed in the normal lung but were decreased or lost In the corresponding tumor tissue of a non small cell lung carcinoma patlent@The luck of expression of six magnet assisted subtraction technique eDNA clones in three additional non-small cell lung cardnoma cases indicates their possible relevance for non-small cell lung carcinoma. Two eDNA clones revealed homology to genes ape cifically expressed in lung, @e., pulmonary surfactant-associated protein B and the receptor for advanced glycosylation end products of proteins. Three cDNA clones showed identity to eDNA sequences encoding cal modulin-like protein, glutamine synthetase, and cytoskeletal 13-actln.One cDNA clone is identical to a recently described human expressed sequence tag whose gene is still unknown.

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“…These insights brought renewed attention to the study of metabolic pathways involved in tumor growth. Medina and colleagues were the first to discuss the role of glutamine metabolism in cancer [45], but only recently, DeBerardinis et al have observed that transformed cells rely on glutamine metabolism to support the synthesis of protein and nucleotides, despite aerobic glycolysis. By using a 13 CNMR spectroscopy technique to study gliomas, the authors showed the catabolic fate Tumor Biol.…”

Section: Glutamine: Paradoxical Roles In Cancer Metabolismmentioning

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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Relevance of glutamine metabolism to tumor cell growth

Cited by 170 publications

References 104 publications

Activation of a system A amino acid transporter, ATA1/SLC38A1, in human hepatocellular carcinoma and preneoplastic liver tissues

Activation of a system A amino acid transporter, ATA1/SLC38A1, in human hepatocellular carcinoma and preneoplastic liver tissues

Identification of genes differentially expressed in normal lung and non-small cell lung carcinoma tissue

Glutamine at focus: versatile roles in cancer

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