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Cancer & Metabolism

Menghan Liu, Lake-Ee Quek, Ghazal Sultani, Nigel Turner
BACKGROUND: Pancreatic ductal adenocarcinoma (PDAC) is a common malignancy with dismal prognosis. Metastatic spread and therapeutic resistance, the main causes of PDAC-related mortalities, are both partially underlined by the epithelial-mesenchymal transition (EMT) of PDAC cells. While the role of Warburg metabolism has been recognized in supporting rapid cellular growth and proliferation in many cancer types, less is known about the metabolic changes occurring during EMT, particularly in the context of PDAC...
2016: Cancer & Metabolism
Stephanie Sprowl-Tanio, Amber N Habowski, Kira T Pate, Miriam M McQuade, Kehui Wang, Robert A Edwards, Felix Grun, Yung Lyou, Marian L Waterman
BACKGROUND: There is increasing evidence that oncogenic Wnt signaling directs metabolic reprogramming of cancer cells to favor aerobic glycolysis or Warburg metabolism. In colon cancer, this reprogramming is due to direct regulation of pyruvate dehydrogenase kinase 1 (PDK1) gene transcription. Additional metabolism genes are sensitive to Wnt signaling and exhibit correlative expression with PDK1. Whether these genes are also regulated at the transcriptional level, and therefore a part of a core metabolic gene program targeted by oncogenic WNT signaling, is not known...
2016: Cancer & Metabolism
Laura M Lashinger, Ciara H O'Flanagan, Sarah M Dunlap, Audrey J Rasmussen, Shannon Sweeney, Jessie Yangxiang Guo, Alessia Lodi, Stefano Tiziani, Eileen White, Stephen D Hursting
BACKGROUND: Calorie restriction (CR) prevents obesity and exerts anticancer effects in many preclinical models. CR is also increasingly being used in cancer patients as a sensitizing strategy prior to chemotherapy regimens. While the beneficial effects of CR are widely accepted, the mechanisms through which CR affects tumor growth are incompletely understood. In many cell types, CR and other nutrient stressors can induce autophagy, which provides energy and metabolic substrates critical for cancer cell survival...
2016: Cancer & Metabolism
Sergey Tumanov, Vinay Bulusu, Eyal Gottlieb, Jurre J Kamphorst
BACKGROUND: Acetyl-CoA is a key metabolic intermediate with roles in the production of energy and biomass, as well as in metabolic regulation. It was recently found that acetate is crucial for maintaining acetyl-CoA production in hypoxic cancer cells. However, the availability of free acetate in the tumor environment and how much tumor cells consume remains unknown. Similarly, much is still to be learned about changes in the dynamics and distribution of acetylation in response to tumor-relevant conditions...
2016: Cancer & Metabolism
Mark A Keibler, Thomas M Wasylenko, Joanne K Kelleher, Othon Iliopoulos, Matthew G Vander Heiden, Gregory Stephanopoulos
BACKGROUND: The study of cancer metabolism has been largely dedicated to exploring the hypothesis that oncogenic transformation rewires cellular metabolism to sustain elevated rates of growth and division. Intense examination of tumors and cancer cell lines has confirmed that many cancer-associated metabolic phenotypes allow robust growth and survival; however, little attention has been given to explicitly identifying the biochemical requirements for cell proliferation in a rigorous manner in the context of cancer metabolism...
2016: Cancer & Metabolism
Michelle A C Reed, Christian Ludwig, Christopher M Bunce, Farhat L Khanim, Ulrich L Günther
BACKGROUND: The role of anaplerotic nutrient entry into the Krebs cycle via pyruvate carboxylase has been the subject of increased scrutiny and in particular whether this is dysregulated in cancer. Here, we use a tracer-based NMR analysis involving high-resolution (1)H-(13)C-HSQC spectra to assess site-specific label incorporation into a range of metabolite pools, including malate, aspartate and glutamate in the acute myeloid leukaemia cell line K562. We also determine how this is affected following treatment with the redeployed drug combination of the lipid-regulating drug bezafibrate and medroxyprogesterone (BaP)...
2016: Cancer & Metabolism
Johannes C van der Mijn, David J Panka, Andrew K Geissler, Henk M Verheul, James W Mier
Molecular profiling studies of tumor tissue from patients with clear cell renal cell cancer (ccRCC) have revealed extensive metabolic reprogramming in this disease. Associations were found between metabolic reprogramming, histopathologic Fuhrman grade, and overall survival of patients. Large-scale genomics, proteomics, and metabolomic analyses have been performed to identify the molecular players in this process. Genes involved in glycolysis, the pentose phosphate pathway, glutamine metabolism, and lipogenesis were found to be upregulated in renal cell cancer (RCC) specimens as compared to normal tissue...
2016: Cancer & Metabolism
Lake-Ee Quek, Menghan Liu, Sanket Joshi, Nigel Turner
BACKGROUND: Glucose and glutamine are the two dominant metabolic substrates in cancer cells. In (13)C tracer experiments, however, it is necessary to account for all significant input substrates, as some natural (unlabelled) substrate in the medium, often derived from serum, can be metabolised by cells despite not showing signs of net consumption. RESULTS: Using [U-(13)C6]-glucose tracers and measuring extracellular metabolite enrichments by GC-MS, we found that pancreatic cells HPDE and PANC-1 secrete lactate, pyruvate, TCA cycle metabolites and non-essential amino acids synthesised from glucose...
2016: Cancer & Metabolism
Tonje H Haukaas, Leslie R Euceda, Guro F Giskeødegård, Santosh Lamichhane, Marit Krohn, Sandra Jernström, Miriam R Aure, Ole C Lingjærde, Ellen Schlichting, Øystein Garred, Eldri U Due, Gordon B Mills, Kristine K Sahlberg, Anne-Lise Børresen-Dale, Tone F Bathen
BACKGROUND: The heterogeneous biology of breast cancer leads to high diversity in prognosis and response to treatment, even for patients with similar clinical diagnosis, histology, and stage of disease. Identifying mechanisms contributing to this heterogeneity may reveal new cancer targets or clinically relevant subgroups for treatment stratification. In this study, we have merged metabolite, protein, and gene expression data from breast cancer patients to examine the heterogeneity at a molecular level...
2016: Cancer & Metabolism
Dustin G Brown, Sangeeta Rao, Tiffany L Weir, Joanne O'Malia, Marlon Bazan, Regina J Brown, Elizabeth P Ryan
BACKGROUND: Colorectal cancers (CRC) are associated with perturbations in cellular amino acids, nucleotides, pentose-phosphate pathway carbohydrates, and glycolytic, gluconeogenic, and tricarboxylic acid intermediates. A non-targeted global metabolome approach was utilized for exploring human CRC, adjacent mucosa, and stool. In this pilot study, we identified metabolite profile differences between CRC and adjacent mucosa from patients undergoing colonic resection. Metabolic pathway analyses further revealed relationships between complex networks of metabolites...
2016: Cancer & Metabolism
Ilinca Georgescu, Robert J Gooding, R Christopher Doiron, Andrew Day, Shamini Selvarajah, Chris Davidson, David M Berman, Paul C Park
BACKGROUND: Gleason scores (GS) 3+3 and 3+4 prostate cancers (PCa) differ greatly in their clinical courses, with Gleason pattern (GP) 4 representing a major independent risk factor for cancer progression. However, Gleason grade is not reliably ascertained by diagnostic biopsy, largely due to sampling inadequacies, subjectivity in the Gleason grading procedure, and a lack of more objective biomarker assays to stratify prostate cancer aggressiveness. In most aggressive cancer types, the tumor microenvironment exhibits a reciprocal pro-tumorigenic metabolic phenotype consistent with the reverse Warburg effect (RWE)...
2016: Cancer & Metabolism
Stacey L Borrego, Johannes Fahrmann, Rupsa Datta, Chiara Stringari, Dmitry Grapov, Michael Zeller, Yumay Chen, Ping Wang, Pierre Baldi, Enrico Gratton, Oliver Fiehn, Peter Kaiser
BACKGROUND: The majority of cancer cells have a unique metabolic requirement for methionine that is not observed in normal, non-tumorigenic cells. This phenotype is described as "methionine dependence" or "methionine stress sensitivity" in which cancer cells are unable to proliferate when methionine has been replaced with its metabolic precursor, homocysteine, in cell culture growth media. We focus on the metabolic response to methionine stress in the triple negative breast cancer cell line MDA-MB-468 and its methionine insensitive derivative cell line MDA-MB-468res-R8...
2016: Cancer & Metabolism
Daniel Weindl, Thekla Cordes, Nadia Battello, Sean C Sapcariu, Xiangyi Dong, Andre Wegner, Karsten Hiller
BACKGROUND: Metabolism gained increasing interest for the understanding of diseases and to pinpoint therapeutic intervention points. However, classical metabolomics techniques only provide a very static view on metabolism. Metabolic flux analysis methods, on the other hand, are highly targeted and require detailed knowledge on metabolism beforehand. RESULTS: We present a novel workflow to analyze non-targeted metabolome-wide stable isotope labeling data to detect metabolic flux changes in a non-targeted manner...
2016: Cancer & Metabolism
Behjatolah Monzavi-Karbassi, Rhonda Gentry, Varinder Kaur, Eric R Siegel, Fariba Jousheghany, Srikanth Medarametla, Barbara J Fuhrman, A Mazin Safar, Laura F Hutchins, Thomas Kieber-Emmons
BACKGROUND: The effect of moderately elevated blood glucose levels among non-diabetic subjects on cancer prognosis is not well described. The goal of this study was to examine the association of elevated random blood glucose (RBG) levels in non-diabetic breast cancer patients with overall survival (OS) and time to tumor recurrence (TTR). RESULTS: Forty-nine deaths and 32 recurrences occurred among 148 eligible study subjects during 855.44 person-years of follow-up, with median follow-up of 5...
2016: Cancer & Metabolism
Barrie Peck, Zachary T Schug, Qifeng Zhang, Beatrice Dankworth, Dylan T Jones, Elizabeth Smethurst, Rachana Patel, Susan Mason, Ming Jiang, Rebecca Saunders, Michael Howell, Richard Mitter, Bradley Spencer-Dene, Gordon Stamp, Lynn McGarry, Daniel James, Emma Shanks, Eric O Aboagye, Susan E Critchlow, Hing Y Leung, Adrian L Harris, Michael J O Wakelam, Eyal Gottlieb, Almut Schulze
BACKGROUND: Enhanced macromolecule biosynthesis is integral to growth and proliferation of cancer cells. Lipid biosynthesis has been predicted to be an essential process in cancer cells. However, it is unclear which enzymes within this pathway offer the best selectivity for cancer cells and could be suitable therapeutic targets. RESULTS: Using functional genomics, we identified stearoyl-CoA desaturase (SCD), an enzyme that controls synthesis of unsaturated fatty acids, as essential in breast and prostate cancer cells...
2016: Cancer & Metabolism
Susan J Gelman, Gary J Patti
No abstract text is available yet for this article.
2016: Cancer & Metabolism
Angela M Otto
Virtually everyone working in cancer research is familiar with the "Warburg effect", i.e., anaerobic glycolysis in the presence of oxygen in tumor cells. However, few people nowadays are aware of what lead Otto Warburg to the discovery of this observation and how his other scientific contributions are seminal to our present knowledge of metabolic and energetic processes in cells. Since science is a human endeavor, and a scientist is imbedded in a network of social and academic contacts, it is worth taking a glimpse into the biography of Otto Warburg to illustrate some of these influences and the historical landmarks in his life...
2016: Cancer & Metabolism
Joerg Martin Buescher, Edward M Driggers
Genome scale data on biological systems has increasingly become available by sequencing of DNA and RNA, and by mass spectrometric quantification of proteins and metabolites. The cellular components from which these -omics regimes are derived act as one integrated system in vivo; thus, there is a natural instinct to integrate -omics data types. Statistical analyses, the use of previous knowledge in the form of networks, and the use of time-resolved measurements are three key design elements for life scientists to consider in planning integrated -omics studies...
2016: Cancer & Metabolism
Nadia Battello, Andreas David Zimmer, Carole Goebel, Xiangyi Dong, Iris Behrmann, Claude Haan, Karsten Hiller, Andre Wegner
BACKGROUND: Hypoxia and inflammation have been identified as hallmarks of cancer. A majority of hepatocellular carcinomas are preceded by hepatitis B- or C-related chronic infections suggesting that liver cancer development is promoted by an inflammatory microenvironment. The inflammatory cytokine oncostatin M (OSM) was shown to induce the expression of hypoxia-inducible factor-1 α (HIF-1 α) under normoxic conditions in hepatocytes and hepatoma cells. HIF-1 α is known to orchestrate the expression of numerous genes, many of which code for metabolic enzymes that play key roles in the adaptation of cellular metabolism to low oxygen tension...
2016: Cancer & Metabolism
Elke Katrin Markert, Alexei Vazquez
Metabolism is essential for life, and its alteration is implicated in multiple human diseases. The transformation from a normal to a cancerous cell requires metabolic changes to fuel the high metabolic demands of cancer cells, including but not limited to cell proliferation and cell migration. In recent years, there have been a number of new discoveries connecting known aberrations in oncogenic and tumour suppressor pathways with metabolic alterations required to sustain cell proliferation and migration. However, an understanding of the selective advantage of these metabolic alterations is still lacking...
2015: Cancer & Metabolism
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