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Glutamine cancer

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https://www.readbyqxmd.com/read/28433662/iron-and-thiol-redox-signaling-in-cancer-an-exquisite-balance-to-escape-ferroptosis
#1
REVIEW
Shinya Toyokuni, Fumiya Ito, Kyoko Yamashita, Yasumasa Okazaki, Shinya Akatsuka
Epidemiological data indicate a constant worldwide increase in cancer mortality, although the age of onset is increasing. Recent accumulation of genomic data on human cancer via next-generation sequencing confirmed that cancer is a disease of genome alteration. In many cancers, the Nrf2 transcription system is activated via mutations either in Nrf2 or Keap1 ubiquitin ligase, leading to persistent activation of the genes with antioxidative functions. Furthermore, deep sequencing of passenger mutations is clarifying responsible cancer causative agent(s) in each case, including aging, APOBEC activation, smoking and UV...
April 19, 2017: Free Radical Biology & Medicine
https://www.readbyqxmd.com/read/28432125/sequential-adaptive-changes-in-a-c-myc-driven-model-of-hepatocellular-carcinoma
#2
James M Dolezal, Huabo Wang, Sucheta Kulkarni, Laura Jackson, Jie Lu, Sarangarajan Ranganathan, Eric S Goetzman, Sivakama Bharathi, Kevin Beezhold, Craig A Byersdorfer, Edward V Prochownik
Hepatocellular carcinoma (HCC) is a common cancer that frequently over-expresses the c-Myc (Myc) oncoprotein. Using a mouse model of Myc-induced HCC, we studied the metabolic, biochemical and molecular changes accompanying HCC progression, regression and recurrence. These involved altered rates of pyruvate and fatty acid β-oxidation and the likely re-directing of glutamine into biosynthetic rather than energy-generating pathways. Initial tumors also showed reduced mitochondrial mass and differential contributions of electron transport chain Complexes I and II to respiration...
April 21, 2017: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/28429737/the-glutamate-cystine-xct-antiporter-antagonizes-glutamine-metabolism-and-reduces-nutrient-flexibility
#3
Chun-Shik Shin, Prashant Mishra, Jeramie D Watrous, Valerio Carelli, Marilena D'Aurelio, Mohit Jain, David C Chan
As noted by Warburg, many cancer cells depend on the consumption of glucose. We performed a genetic screen to identify factors responsible for glucose addiction and recovered the two subunits of the xCT antiporter (system xc(-)), which plays an antioxidant role by exporting glutamate for cystine. Disruption of the xCT antiporter greatly improves cell viability after glucose withdrawal, because conservation of glutamate enables cells to maintain mitochondrial respiration. In some breast cancer cells, xCT antiporter expression is upregulated through the antioxidant transcription factor Nrf2 and contributes to their requirement for glucose as a carbon source...
April 21, 2017: Nature Communications
https://www.readbyqxmd.com/read/28427169/therapeutic-role-of-glutamine-in-management-of-radiation-enteritis-a-meta-analysis-of-13-randomized-controlled-trials
#4
REVIEW
De-Dong Cao, Hui-Lin Xu, Min Xu, Xiang-Yun Qian, Zhu-Cheng Yin, Wei Ge
OBJECTIVE: To systematically evaluate the clinical efficacy of glutamine in treating radiation enteritis in cancer patients treated with radiotherapy. METHODS: Electronic databases including Pubmed, Embase, the Cochrane library, and CNKI were systematically searched, until April 2016. Randomized controlled trials (RCT) of glutamine in the treatment of radiation enteritis in cancer patients were searched, and RevMan 5.3 software was used for Meta-analysis. RESULTS: A total of 13 RCTs were included, involving 979 patients...
February 25, 2017: Oncotarget
https://www.readbyqxmd.com/read/28424408/synthetic-lethality-of-glutaminolysis-inhibition-autophagy-inactivation-and-asparagine-depletion-in-colon-cancer
#5
Jiaqiu Li, Ping Song, Liyuan Zhu, Neelum Aziz, Qiyin Zhou, Yulong Zhang, Wenxia Xu, Lifeng Feng, Dingwei Chen, Xian Wang, Hongchuan Jin
Cancer cells reprogram metabolism to coordinate their rapid growth. They addict on glutamine metabolism for adenosine triphosphate generation and macromolecule biosynthesis. In this study, we report that glutamine deprivation retarded cell growth and induced prosurvival autophagy. Autophagy inhibition by chloroquine significantly enhanced glutamine starvation induced growth inhibition and apoptosis activation. Asparagine deprivation by L-asparaginase exacerbated growth inhibition induced by glutamine starvation and autophagy blockage...
April 5, 2017: Oncotarget
https://www.readbyqxmd.com/read/28420743/cancer-cell-metabolism-the-essential-role-of-the-nonessential-amino-acid-glutamine
#6
REVIEW
Ji Zhang, Natalya N Pavlova, Craig B Thompson
Biochemistry textbooks and cell culture experiments seem to be telling us two different things about the significance of external glutamine supply for mammalian cell growth and proliferation. Despite the fact that glutamine is a nonessential amino acid that can be synthesized by cells from glucose-derived carbons and amino acid-derived ammonia, most mammalian cells in tissue culture cannot proliferate or even survive in an environment that does not contain millimolar levels of glutamine. Not only are the levels of glutamine in standard tissue culture media at least ten-fold higher than other amino acids, but glutamine is also the most abundant amino acid in the human bloodstream, where it is assiduously maintained at approximately 0...
April 18, 2017: EMBO Journal
https://www.readbyqxmd.com/read/28416685/snat7-is-the-primary-lysosomal-glutamine-exporter-required-for-extracellular-protein-dependent-growth-of-cancer-cells
#7
Quentin Verdon, Marielle Boonen, Christopher Ribes, Michel Jadot, Bruno Gasnier, Corinne Sagné
Lysosomes degrade cellular components sequestered by autophagy or extracellular material internalized by endocytosis and phagocytosis. The macromolecule building blocks released by lysosomal hydrolysis are then exported to the cytosol by lysosomal transporters, which remain undercharacterized. In this study, we designed an in situ assay of lysosomal amino acid export based on the transcription factor EB (TFEB), a master regulator of lysosomal biogenesis that detects lysosomal storage. This assay was used to screen candidate lysosomal transporters, leading to the identification of sodium-coupled neutral amino acid transporter 7 (SNAT7), encoded by the SLC38A7 gene, as a lysosomal transporter highly selective for glutamine and asparagine...
April 17, 2017: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/28414307/metabolic-inhibitors-accentuate-the-anti-tumoral-effect-of-hdac5-inhibition
#8
E Hendrick, P Peixoto, A Blomme, C Polese, N Matheus, J Cimino, A Frère, A Mouithys-Mickalad, D Serteyn, L Bettendorff, B Elmoualij, P De Tullio, G Eppe, F Dequiedt, V Castronovo, D Mottet
The US FDA approval of broad-spectrum histone deacetylase (HDAC) inhibitors has firmly laid the cancer community to explore HDAC inhibition as a therapeutic approach for cancer treatment. Hitting one HDAC member could yield clinical benefit but this required a complete understanding of the functions of the different HDAC members. Here we explored the consequences of specific HDAC5 inhibition in cancer cells. We demonstrated that HDAC5 inhibition induces an iron-dependent reactive oxygen species (ROS) production, ultimately leading to apoptotic cell death as well as mechanisms of mitochondria quality control (mitophagy and mitobiogenesis)...
April 17, 2017: Oncogene
https://www.readbyqxmd.com/read/28408437/the-myc-mrna-3-utr-couples-rna-polymerase-ii-function-to-glutamine-and-ribonucleotide-levels
#9
Francesca R Dejure, Nadine Royla, Steffi Herold, Jacqueline Kalb, Susanne Walz, Carsten P Ade, Guido Mastrobuoni, Jens T Vanselow, Andreas Schlosser, Elmar Wolf, Stefan Kempa, Martin Eilers
Deregulated expression of MYC enhances glutamine utilization and renders cell survival dependent on glutamine, inducing "glutamine addiction". Surprisingly, colon cancer cells that express high levels of MYC due to WNT pathway mutations are not glutamine-addicted but undergo a reversible cell cycle arrest upon glutamine deprivation. We show here that glutamine deprivation suppresses translation of endogenous MYC via the 3'-UTR of the MYC mRNA, enabling escape from apoptosis. This regulation is mediated by glutamine-dependent changes in adenosine-nucleotide levels...
April 13, 2017: EMBO Journal
https://www.readbyqxmd.com/read/28400509/oncogene-kras-activates-fatty-acid-synthase-resulting-in-specific-erk-and-lipid-signatures-associated-with-lung-adenocarcinoma
#10
Arvin M Gouw, Livia S Eberlin, Katherine Margulis, Delaney K Sullivan, Georgia G Toal, Ling Tong, Richard N Zare, Dean W Felsher
KRAS gene mutation causes lung adenocarcinoma. KRAS activation has been associated with altered glucose and glutamine metabolism. Here, we show that KRAS activates lipogenesis, and this activation results in distinct proteomic and lipid signatures. By gene expression analysis, KRAS is shown to be associated with a lipogenesis gene signature and specific induction of fatty acid synthase (FASN). Through desorption electrospray ionization MS imaging (DESI-MSI), specific changes in lipogenesis and specific lipids are identified...
April 11, 2017: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/28400476/gad1-upregulation-programs-aggressive-features-of-cancer-cell-metabolism-in-the-brain-metastatic-microenvironment
#11
Patricia M Schnepp, Dennis D Lee, Ian H Guldner, Treasa K O'Tighearnaigh, Erin N Howe, Bhavana Palakurthi, Kaitlyn E Eckert, Tiffany A Toni, Brandon L Ashfeld, Siyuan Zhang
The impact of altered amino acid metabolism on cancer progression is not fully understood. We hypothesized that a metabolic transcriptome shift during metastatic evolution is crucial for brain metastasis. Here we report a powerful impact in this setting caused by epigenetic upregulation of glutamate decarboxylase 1 (GAD1), a regulator of the GABA neurotransmitter metabolic pathway. In cell-based culture and brain metastasis models, we found that downegulation of the DNA methyltransferase DNMT1 induced by the brain microenvironment-derived clusterin resulted in decreased GAD1 promoter methylation and subsequent upregulation of GAD1 expression in brain metastatic tumor cells...
April 11, 2017: Cancer Research
https://www.readbyqxmd.com/read/28399896/glutaminase-1-plays-a-key-role-in-the-cell-growth-of-fibroblast-like-synoviocytes-in-rheumatoid-arthritis
#12
Soshi Takahashi, Jun Saegusa, Sho Sendo, Takaichi Okano, Kengo Akashi, Yasuhiro Irino, Akio Morinobu
BACKGROUND: The recent findings of cancer-specific metabolic changes, including increased glucose and glutamine consumption, have provided new therapeutic targets for consideration. Fibroblast-like synoviocytes (FLS) from rheumatoid arthritis (RA) patients exhibit several tumor cell-like characteristics; however, the role of glucose and glutamine metabolism in the aberrant proliferation of these cells is unclear. Here, we evaluated the role of these metabolic pathways in RA-FLS proliferation and in autoimmune arthritis in SKG mice...
April 11, 2017: Arthritis Research & Therapy
https://www.readbyqxmd.com/read/28399876/emerging-roles-of-lipid-metabolism-in-cancer-metastasis
#13
REVIEW
Xiangjian Luo, Can Cheng, Zheqiong Tan, Namei Li, Min Tang, Lifang Yang, Ya Cao
Cancer cells frequently display fundamentally altered cellular metabolism, which provides the biochemical foundation and directly contributes to tumorigenicity and malignancy. Rewiring of metabolic programmes, such as aerobic glycolysis and increased glutamine metabolism, are crucial for cancer cells to shed from a primary tumor, overcome the nutrient and energy deficit, and eventually survive and form metastases. However, the role of lipid metabolism that confers the aggressive properties of malignant cancers remains obscure...
April 11, 2017: Molecular Cancer
https://www.readbyqxmd.com/read/28394261/folate-cycle-enzyme-mthfd1l-confers-metabolic-advantages-in-hepatocellular-carcinoma
#14
Derek Lee, Iris Ming-Jing Xu, David Kung-Chun Chiu, Robin Kit-Ho Lai, Aki Pui-Wah Tse, Lynna Lan Li, Cheuk-Ting Law, Felice Ho-Ching Tsang, Larry Lai Wei, Cerise Yuen-Ki Chan, Chun-Ming Wong, Irene Oi-Lin Ng, Carmen Chak-Lui Wong
Cancer cells preferentially utilize glucose and glutamine, which provide macromolecules and antioxidants that sustain rapid cell division. Metabolic reprogramming in cancer drives an increased glycolytic rate that supports maximal production of these nutrients. The folate cycle, through transfer of a carbon unit between tetrahydrofolate and its derivatives in the cytoplasmic and mitochondrial compartments, produces other metabolites that are essential for cell growth, including nucleotides, methionine, and the antioxidant NADPH...
April 10, 2017: Journal of Clinical Investigation
https://www.readbyqxmd.com/read/28393905/metabolomic-characterisation-of-the-effects-of-oncogenic-pik3ca-transformation-in-a-breast-epithelial-cell-line
#15
Chung-Ho E Lau, Gregory D Tredwell, James K Ellis, Eric W-F Lam, Hector C Keun
Somatic mutations in PIK3CA are frequently found in a number of human cancers, including breast cancer, altering cellular physiology and tumour sensitivity to chemotherapy. This renders PIK3CA an attractive molecular target for early detection and personalised therapy. Using (1)H Nuclear Magnetic Resonance spectroscopy (NMR) and Gas Chromatography - Mass Spectrometery (GC-MS) together with (13)C stable isotope-labelled glucose and glutamine as metabolic tracers, we probed the phenotypic changes in metabolism following a single copy knock-in of mutant PIK3CA (H1047R) in the MCF10A cell line, an important cell model for studying oncogenic transformation in breast tissues...
April 10, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28393186/a-novel-5-fluorouracil-resistant-human-esophageal-squamous-cell-carcinoma-cell-line-eca-109-5-fu-with-significant-drug-resistance-related-characteristics
#16
Chi Zhang, Qunfeng Ma, Yinan Shi, Xue Li, Ming Wang, Junfeng Wang, Jianlin Ge, Zhinan Chen, Ziling Wang, Hong Jiang
5-Fluorouracil (5-FU) is used for the clinical treatment of esophageal squamous cell carcinomas (ESCCs), yet it also induces chemoresistant cancer cells during treatment, which leads to the failure of the therapy. To further explore the resistance mechanism of 5-FU in ESCC, we established the 5-FU-resistant ESCC cell line Eca-109/5-FU, which was prepared by the stepwise exposure to increasing 5-FU concentrations. MTT assay and nude mouse xenograft models were used to test the drug resistance and proliferation of Eca-109 and Eca-109/5-FU cells in vitro and in vivo...
March 31, 2017: Oncology Reports
https://www.readbyqxmd.com/read/28393116/glutamine-metabolism-in-cancer-understanding-the-heterogeneity
#17
Ahmad A Cluntun, Michael J Lukey, Richard A Cerione, Jason W Locasale
Reliance on glutamine has long been considered a hallmark of cancer cell metabolism. However, some recent studies have challenged this notion in vivo, prompting a need for further clarifications on the role of glutamine metabolism in cancer. We find that there is ample evidence of an essential role for glutamine in tumors and that a variety of factors, including tissue type, the underlying cancer genetics, the tumor microenvironment and other variables such as diet and host physiology collectively influence the role of glutamine in cancer...
March 2017: Trends in Cancer
https://www.readbyqxmd.com/read/28390870/insulin-not-glutamine-dipeptide-reduces-lipases-expression-and-prevents-fat-wasting-and-weight-loss-in-walker-256-tumor-bearing-rats
#18
Hely de Morais, Flaviane de Fatima Silva, Francemilson Goulart da Silva, Milene Ortiz Silva, Maria Fernanda Rodrigues Graciano, Maria Isabel Lovo Martins, Ângelo Rafael Carpinelli, Tânia Longo Mazucco, Roberto Barbosa Bazotte, Helenir Medri de Souza
Cachexia is the main cause of mortality in advanced cancer patients. We investigated the effects of insulin (INS) and glutamine dipeptide (GDP), isolated or associated, on cachexia and metabolic changes induced by Walker 256 tumor in rats. INS (NPH, 40 UI/kg, sc) or GDP (1.5g/kg, oral gavage) was once-daily administered during 11 days after tumor cell inoculation. GDP, INS or INS+GDP treatments did not influence the tumor growth. However, INS and INS+GDP prevented retroperitoneal fat wasting and body weight loss of tumor-bearing rats...
April 6, 2017: European Journal of Pharmacology
https://www.readbyqxmd.com/read/28388380/acquired-amino-acid-deficiencies-a-focus-on-arginine-and-glutamine
#19
Claudia R Morris, Jill Hamilton-Reeves, Robert G Martindale, Menaka Sarav, Juan B Ochoa Gautier
Nonessential amino acids are synthesized de novo and therefore not diet dependent. In contrast, essential amino acids must be obtained through nutrition since they cannot be synthesized internally. Several nonessential amino acids may become essential under conditions of stress and catabolic states when the capacity of endogenous amino acid synthesis is exceeded. Arginine and glutamine are 2 such conditionally essential amino acids and are the focus of this review. Low arginine bioavailability plays a pivotal role in the pathogenesis of a growing number of varied diseases, including sickle cell disease, thalassemia, malaria, acute asthma, cystic fibrosis, pulmonary hypertension, cardiovascular disease, certain cancers, and trauma, among others...
April 2017: Nutrition in Clinical Practice
https://www.readbyqxmd.com/read/28378915/structure-of-6-diazo-5-oxo-norleucine-bound-human-gamma-glutamyl-transpeptidase-1-a-novel-mechanism-of-inactivation
#20
Simon S Terzyan, Paul F Cook, Annie Heroux, Marie H Hanigan
Intense efforts are underway to identify inhibitors of the enzyme gamma-glutamyl transpeptidase 1 (GGT1) which cleaves extracellular gamma-glutamyl compounds and contributes to the pathology of asthma, reperfusion injury and cancer. The glutamate analog, 6-diazo-5-oxo-norleucine (DON), inhibits GGT1. DON also inhibits many essential glutamine metabolizing enzymes rendering it too toxic for use in the clinic as a GGT1 inhibitor. We investigated the molecular mechanism of human GGT1 (hGGT1) inhibition by DON to determine possible strategies for increasing its specificity for hGGT1...
April 5, 2017: Protein Science: a Publication of the Protein Society
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