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Cancer AND glutamine

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https://www.readbyqxmd.com/read/28531452/the-effect-of-glutamine-and-arginine-enriched-nutritional-support-on-quality-of-life-in-head-and-neck-cancer-patients-treated-with-imrt
#1
Sezin Yuce Sari, Gozde Yazici, Deniz Yuce, Erdem Karabulut, Mustafa Cengiz, Gokhan Ozyigit
BACKGROUND AND AIMS: Oral mucositis and esophagitis are common acute toxicities of radiotherapy (RT) for head and neck cancer (HNC). In order to decrease the rates of these toxicities, we compared quality of life in HNC patients that did and did not receive a glutamine and arginine-enriched solution (GAES) during RT. METHODS: A total of 29 patients received intensity-modulated radiotherapy (IMRT); 15 used GAES b.i.d. during the treatment, and a matched cohort of 14 patients did not...
December 2016: Clinical Nutrition ESPEN
https://www.readbyqxmd.com/read/28526133/metabolic-reprogramming-and-oncogenesis-one-hallmark-many-organelles
#2
A S H Costa, C Frezza
The process of tumorigenesis can be described by a series of molecular features, among which alteration of cellular metabolism has recently emerged. This metabolic rewiring fulfills the energy and biosynthetic demands of fast proliferating cancer cells and amplifies their metabolic repertoire to survive and proliferate in the poorly oxygenated and nutrient-deprived tumor microenvironment. During the last decade, the complex reprogramming of cancer cell metabolism has been widely investigated, revealing cancer-specific metabolic alterations...
2017: International Review of Cell and Molecular Biology
https://www.readbyqxmd.com/read/28525376/exploiting-ros-and-metabolic-differences-to-kill-cisplatin-resistant-lung-cancer
#3
Medhi Wangpaichitr, Chunjing Wu, Ying Ying Li, Dan J M Nguyen, Hande Kandemir, Sumedh Shah, Shumei Chen, Lynn G Feun, Jeffrey S Prince, Macus T Kuo, Niramol Savaraj
Cisplatin resistance remains a major problem in the treatment of lung cancer. We have discovered that cisplatin resistant (CR) lung cancer cells, regardless of the signaling pathway status, share the common parameter which is an increase in reactive oxygen species (ROS) and undergo metabolic reprogramming. CR cells were no longer addicted to the glycolytic pathway, but rather relied on oxidative metabolism. They took up twice as much glutamine and were highly sensitive to glutamine deprivation. Glutamine is hydrolyzed to glutamate for glutathione synthesis, an essential factor to abrogate high ROS via xCT antiporter...
May 2, 2017: Oncotarget
https://www.readbyqxmd.com/read/28516268/gpna-inhibits-the-sodium-independent-transport-system-l-for-neutral-amino-acids
#4
Martina Chiu, Cosimo Sabino, Giuseppe Taurino, Massimiliano G Bianchi, Roberta Andreoli, Nicola Giuliani, Ovidio Bussolati
L-γ-Glutamyl-p-nitroanilide (GPNA) is widely used to inhibit the glutamine transporter ASCT2, although it is known that it also inhibits other sodium-dependent amino acid transporters. In a panel of human cancer cell lines, which express the system L transporters LAT1 and LAT2, GPNA inhibits the sodium-independent influx of leucine and glutamine. The kinetics of the effect suggests that GPNA is a low affinity, competitive inhibitor of system L transporters. In Hs683 human oligodendroglioma cells, the incubation in the presence of GPNA, but not ASCT2 silencing, lowers the cell content of leucine...
May 17, 2017: Amino Acids
https://www.readbyqxmd.com/read/28507224/c-myc-mrna-tail-tale-about-glutamine-control-of-transcription
#5
Chi V Dang
Dejure et al (2017) demonstrates an intriguing link between glutamine, c-MYC protein levels, and c-MYC-dependent transcription. Glutamine-dependent c-MYC protein level, which is sensed through the c-MYC mRNA 3'-UTR, determines global transcriptional response to glutamine deprivation in HCT116 colon cancer cells. These findings add another layer of complexity to c-MYC's role as a nexus in metabolic regulation.
May 15, 2017: EMBO Journal
https://www.readbyqxmd.com/read/28507054/glutamine-transporters-are-targets-of-multiple-oncogenic-signaling-pathways-in-prostate-cancer
#6
Mark A White, Chenchu Lin, Kimal Rajapakshe, Jianrong Dong, Yan Shi, Efrosini Tsouko, Ratna Mukhopadhyay, Diana Jasso, Wajahat Dawood, Cristian Coarfa, Daniel E Frigo
Despite the known importance of androgen receptor (AR) signaling in prostate cancer (PCa), the processes downstream of AR that drive disease development and progression remain poorly understood. This knowledge gap has thus limited the ability to treat cancer. Here, it is demonstrated that androgens increase the metabolism of glutamine in PCa cells. This metabolism was required for maximal cell growth under conditions of serum starvation. Mechanistically, AR signaling promoted glutamine metabolism by increasing the expression of the glutamine transporters SLC1A4 and SLC1A5, genes commonly overexpressed in PCa...
May 15, 2017: Molecular Cancer Research: MCR
https://www.readbyqxmd.com/read/28496003/peiminine-inhibits-colorectal-cancer-cell-proliferation-by-inducing-apoptosis-and-autophagy-and-modulating-key-metabolic-pathways
#7
Zhi Zheng, Liting Xu, Shuofeng Zhang, Wuping Li, Fangfang Tou, Qinsi He, Jun Rao, Qiang Shen
Peiminine, a compound extracted from the bulbs of Fritillaria thunbergii and traditionally used as a medication in China and other Asian countries, was reported to inhibit colorectal cancer cell proliferation and tumor growth by inducing autophagic cell death. However, its mechanism of anticancer action is not well understood, especially at the metabolic level, which was thought to primarily account for peiminine's efficacy against cancer. Using an established metabolomic profiling platform combining ultra-performance liquid chromatography/tandem mass spectrometry with gas chromatography/mass spectrometry, we identified metabolic alterations in colorectal cancer cell line HCT-116 after peiminine treatment...
April 25, 2017: Oncotarget
https://www.readbyqxmd.com/read/28481367/inhibition-of-malic-enzyme-1-disrupts-cellular-metabolism-and-leads-to-vulnerability-in-cancer-cells-in-glucose-restricted-conditions
#8
S Murai, A Ando, S Ebara, M Hirayama, Y Satomi, T Hara
Malic enzyme 1 (ME1) regulates one of the main pathways that provide nicotinamide adenine dinucleotide phosphate (NADPH), which is essential for cancer cell growth through maintenance of redox balance and biosynthesis processes in the cytoplasm. In this study, we found that ME1 inhibition disrupted metabolism in cancer cells and inhibited cancer cell growth by inducing senescence or apoptosis. In glucose-restricted culture conditions, cancer cells increased ME1 expression, and tracer experiments with labelled glutamine revealed that the flux of ME1-derived pyruvate to citrate was enhanced...
May 8, 2017: Oncogenesis
https://www.readbyqxmd.com/read/28480903/metabolic-reprogramming-in-clear-cell-renal-cell-carcinoma
#9
REVIEW
Hiromi I Wettersten, Omran Abu Aboud, Primo N Lara, Robert H Weiss
Research in many cancers has uncovered changes in metabolic pathways that control tumour energetics and biosynthesis, so-called metabolic reprogramming. Studies in clear cell renal cell carcinoma (ccRCC) have been particularly revealing, leading to the concept that ccRCC is a metabolic disease. ccRCC is generally accompanied by reprogramming of glucose and fatty acid metabolism and of the tricarboxylic acid cycle. Metabolism of tryptophan, arginine and glutamine is also reprogrammed in many ccRCCs, and these changes provide opportunities for new therapeutic strategies, biomarkers and imaging modalities...
May 8, 2017: Nature Reviews. Nephrology
https://www.readbyqxmd.com/read/28467910/targeting-ras-driven-cancer-cell-survival-and-invasion-through-selective-inhibition-of-dock1
#10
Hirotada Tajiri, Takehito Uruno, Takahiro Shirai, Daisuke Takaya, Shigeki Matsunaga, Daiki Setoyama, Mayuki Watanabe, Mutsuko Kukimoto-Niino, Kounosuke Oisaki, Miho Ushijima, Fumiyuki Sanematsu, Teruki Honma, Takaho Terada, Eiji Oki, Senji Shirasawa, Yoshihiko Maehara, Dongchon Kang, Jean-François Côté, Shigeyuki Yokoyama, Motomu Kanai, Yoshinori Fukui
Oncogenic Ras plays a key role in cancer initiation but also contributes to malignant phenotypes by stimulating nutrient uptake and promoting invasive migration. Because these latter cellular responses require Rac-mediated remodeling of the actin cytoskeleton, we hypothesized that molecules involved in Rac activation may be valuable targets for cancer therapy. We report that genetic inactivation of the Rac-specific guanine nucleotide exchange factor DOCK1 ablates both macropinocytosis-dependent nutrient uptake and cellular invasion in Ras-transformed cells...
May 2, 2017: Cell Reports
https://www.readbyqxmd.com/read/28464016/muc1-facilitates-metabolomic-reprogramming-in-triple-negative-breast-cancer
#11
Gennifer Goode, Venugopal Gunda, Nina V Chaika, Vinee Purohit, Fang Yu, Pankaj K Singh
BACKGROUND: Mucin1 (MUC1), a glycoprotein associated with chemoresistance and an aggressive cancer phenotype, is aberrantly overexpressed in triple-negative breast cancer (TNBC). Recent studies suggest that MUC1 plays a role in modulating cancer cell metabolism and thereby supports tumor growth. Herein, we examined the role of MUC1 in metabolic reprogramming in TNBC. METHODS: MUC1 was stably overexpressed in MDA-MB-231 TNBC cells and stably knocked down in MDA-MB-468 cells...
2017: PloS One
https://www.readbyqxmd.com/read/28457411/immunoexpression-of-heat-shock-protein-70-glypican-3-glutamine-synthetase-and-beta-catenin-in-hepatocellular-carcinoma-after-liver-transplantation-association-between-positive-glypican-3-and-beta-catenin-with-the-presence-of-larger-nodules
#12
E C Ataide, S R Perales, M G Silva, F C Filho, A C Sparapani, P F Latuf Filho, R S B Stucchi, J Vassallo, C A F Escanhoela, I F S F Boin
BACKGROUND: Hepatocellular carcinoma (HCC) is the 6th leading cause of cancer worldwide. Its recurrence ranges from 6% to 26%. In the literature, many factors are associated with higher risk of recurrence, without a clear definition of the best method that could predict this highly lethal event. OBJECTIVE: The aim of this study was to evaluate the immunoexpression of immunohistochemical markers: HSP70, glypican 3, glutamine synthetase, and beta-catenin, as well as studying their association with tumor characteristics and prognosis of patients undergoing liver transplantation for HCC...
May 2017: Transplantation Proceedings
https://www.readbyqxmd.com/read/28455244/got1-mediated-anaplerotic-glutamine-metabolism-regulates-chronic-acidosis-stress-in-pancreatic-cancer-cells
#13
Jaime Abrego, Venugopal Gunda, Enza Vernucci, Surendra K Shukla, Ryan J King, Aneesha Dasgupta, Gennifer Goode, Divya Murthy, Fang Yu, Pankaj K Singh
The increased rate of glycolysis and reduced oxidative metabolism are the principal biochemical phenotypes observed in pancreatic ductal adenocarcinoma (PDAC) that lead to the development of an acidic tumor microenvironment. The pH of most epithelial cell-derived tumors is reported to be lower than that of plasma. However, little is known regarding the physiology and metabolism of cancer cells enduring chronic acidosis. Here, we cultured PDAC cells in chronic acidosis (pH 6.9-7.0) and observed that cells cultured in low pH had reduced clonogenic capacity...
April 26, 2017: Cancer Letters
https://www.readbyqxmd.com/read/28446878/computational-model-predicts-the-effects-of-targeting-cellular-metabolism-in-pancreatic-cancer
#14
Mahua Roy, Stacey D Finley
Reprogramming of energy metabolism is a hallmark of cancer that enables the cancer cells to meet the increased energetic requirements due to uncontrolled proliferation. One prominent example is pancreatic ductal adenocarcinoma, an aggressive form of cancer with an overall 5-year survival rate of 5%. The reprogramming mechanism in pancreatic cancer involves deregulated uptake of glucose and glutamine and other opportunistic modes of satisfying energetic demands in a hypoxic and nutrient-poor environment. In the current study, we apply systems biology approaches to enable a better understanding of the dynamics of the distinct metabolic alterations in KRAS-mediated pancreatic cancer, with the goal of impeding early cell proliferation by identifying the optimal metabolic enzymes to target...
2017: Frontiers in Physiology
https://www.readbyqxmd.com/read/28443090/immunometabolic-regulations-mediated-by-coinhibitory-receptors-and-their-impact-on-t-cell-immune-responses
#15
REVIEW
Nikolaos Patsoukis, Jessica D Weaver, Laura Strauss, Christoph Herbel, Pankaj Seth, Vassiliki A Boussiotis
Host immunity provides wide spectrum protection that serves to eradicate pathogens and cancer cells, while maintaining self-tolerance and immunological homeostasis. Ligation of the T cell receptor (TCR) by antigen activates signaling pathways that coordinately induce aerobic glycolysis, mitochondrial activity, anabolic metabolism, and T effector cell differentiation. Activation of PI3K, Akt, and mTOR triggers the switch to anabolic metabolism by inducing transcription factors such as Myc and HIF1, and the glucose transporter Glut1, which is pivotal for the increase of glucose uptake after T cell activation...
2017: Frontiers in Immunology
https://www.readbyqxmd.com/read/28441384/hopefully-devoted-to-q-targeting-glutamine-addiction-in-cancer
#16
REVIEW
Emma R Still, Mariia O Yuneva
Altered cell metabolism enables tumours to sustain their increased energetic and biosynthetic needs. Although tumour metabolism has long been considered a promising discipline in the development of cancer therapeutics, the majority of work has focused on changes in glucose metabolism. However, the complexity of cellular metabolism means that very rarely is an individual metabolite required for a single purpose, and thus understanding the overall metabolic requirements of tumours is vital. Over the past 30 years, increasing evidence has shown that many tumours require glutamine as well as glucose for their proliferation and survival...
May 23, 2017: British Journal of Cancer
https://www.readbyqxmd.com/read/28440528/-effect-of-asct2-gene-knock-down-by-shrna-on-biological-behaviors-of-colorectal-cancer-cells
#17
Canfeng Cai, Bing Zeng, Jun Zeng, Haiyang Xin, Chaoming Tang
OBJECTIVE: To investigate the effect of ASCT2 gene (glutamine transporter) knock-down by shRNA on biological behaviors of colorectal cancer cells. METHODS: shRNA was transfected into colorectal cancer cells Lovo and SW480 to knockdown ASCT2 mediated by Lipofectamine 2000. Reverse transcription-PCR and Western blot were used to examine the mRNA and protein expression of ASCT2. MTT and transwell assay were used to determine the proliferation and invasiveness of Lovo and SW480 cells...
April 25, 2017: Zhonghua Wei Chang Wai Ke za Zhi, Chinese Journal of Gastrointestinal Surgery
https://www.readbyqxmd.com/read/28433662/iron-and-thiol-redox-signaling-in-cancer-an-exquisite-balance-to-escape-ferroptosis
#18
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
#19
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
#20
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
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