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Cancer & Metabolism

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https://www.readbyqxmd.com/read/29692895/metabolic-characterization-of-isocitrate-dehydrogenase-idh-mutant-and-idh-wildtype-gliomaspheres-uncovers-cell-type-specific-vulnerabilities
#1
Matthew Garrett, Jantzen Sperry, Daniel Braas, Weihong Yan, Thuc M Le, Jack Mottahedeh, Kirsten Ludwig, Ascia Eskin, Yue Qin, Rachelle Levy, Joshua J Breunig, Frank Pajonk, Thomas G Graeber, Caius G Radu, Heather Christofk, Robert M Prins, Albert Lai, Linda M Liau, Giovanni Coppola, Harley I Kornblum
Background: There is considerable interest in defining the metabolic abnormalities of IDH mutant tumors to exploit for therapy. While most studies have attempted to discern function by using cell lines transduced with exogenous IDH mutant enzyme, in this study, we perform unbiased metabolomics to discover metabolic differences between a cohort of patient-derived IDH1 mutant and IDH wildtype gliomaspheres. Methods: Using both our own microarray and the TCGA datasets, we performed KEGG analysis to define pathways differentially enriched in IDH1 mutant and IDH wildtype cells and tumors...
2018: Cancer & Metabolism
https://www.readbyqxmd.com/read/29619217/metabolomics-of-oncogene-specific-metabolic-reprogramming-during-breast-cancer
#2
Chen Dai, Jennifer Arceo, James Arnold, Arun Sreekumar, Norman J Dovichi, Jun Li, Laurie E Littlepage
Background: The complex yet interrelated connections between cancer metabolism and oncogenic driver genes are relatively unexplored but have the potential to identify novel biomarkers and drug targets with prognostic and therapeutic value. The goal of this study was to identify global metabolic profiles of breast tumors isolated from multiple transgenic mouse models and to identify unique metabolic signatures driven by these oncogenes. Methods: Using mass spectrometry (GC-MS, LC-MS/MS, and capillary zone electrophoresis (CZE)-MS platforms), we quantified and compared the levels of 374 metabolites in breast tissue from normal and transgenic mouse breast cancer models overexpressing a panel of oncogenes (PyMT, PyMT-DB, Wnt1, Neu, and C3-TAg)...
2018: Cancer & Metabolism
https://www.readbyqxmd.com/read/29619216/mutant-idh1-gliomas-downregulate-phosphocholine-and-phosphoethanolamine-synthesis-in-a-2-hydroxyglutarate-dependent-manner
#3
Pavithra Viswanath, Marina Radoul, Jose Luis Izquierdo-Garcia, Hema Artee Luchman, J Gregory Cairncross, Russell O Pieper, Joanna J Phillips, Sabrina M Ronen
Background: Magnetic resonance spectroscopy (MRS) studies have identified elevated levels of the phospholipid precursor phosphocholine (PC) and phosphoethanolamine (PE) as metabolic hallmarks of cancer. Unusually, however, PC and PE levels are reduced in mutant isocitrate dehydrogenase 1 (IDHmut) gliomas that produce the oncometabolite 2-hydroxyglutarate (2-HG) relative to wild-type IDH1 (IDHwt) gliomas. The goal of this study was to determine the molecular mechanism underlying this unusual metabolic reprogramming in IDHmut gliomas...
2018: Cancer & Metabolism
https://www.readbyqxmd.com/read/29568521/elevated-circulatory-levels-of-leptin-and-resistin-impair-therapeutic-efficacy-of-dacarbazine-in-melanoma-under-obese-state
#4
Parmanand Malvi, Balkrishna Chaube, Shivendra Vikram Singh, Naoshad Mohammad, Maleppillil Vavachan Vijayakumar, Snahlata Singh, Surbhi Chouhan, Manoj Kumar Bhat
Background: Obesity is associated with increased risk, poor prognosis and outcome of therapy, in various cancers. Obesity-associated factors or adipokines, especially leptin and resistin, are purported to promote growth, survival, proliferation, and invasiveness of cancer cells. However, the mechanistic link between these adipokines and therapeutic response in malignancies is not clearly understood. Methods: ob/ob and db/db mouse models were used in this study to evaluate the role of leptin and resistin towards the outcome of dacarbazine (DTIC) therapy in melanoma...
2018: Cancer & Metabolism
https://www.readbyqxmd.com/read/29541451/cancer-cell-metabolic-plasticity-allows-resistance-to-nampt-inhibition-but-invariably-induces-dependence-on-ldha
#5
Natthakan Thongon, Chiara Zucal, Vito Giuseppe D'Agostino, Toma Tebaldi, Silvia Ravera, Federica Zamporlini, Francesco Piacente, Ruxanda Moschoi, Nadia Raffaelli, Alessandro Quattrone, Alessio Nencioni, Jean-Francois Peyron, Alessandro Provenzani
Background: Inhibitors of nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme in NAD+ biosynthesis from nicotinamide, exhibit anticancer effects in preclinical models. However, continuous exposure to NAMPT inhibitors, such as FK866, can induce acquired resistance. Methods: We developed FK866-resistant CCRF-CEM (T cell acute lymphoblastic leukemia) and MDA MB231 (breast cancer) models, and by exploiting an integrated approach based on genetic, biochemical, and genome wide analyses, we annotated the drug resistance mechanisms...
2018: Cancer & Metabolism
https://www.readbyqxmd.com/read/29225823/human-mitochondrial-mthfd2-is-a-dual-redox-cofactor-specific-methylenetetrahydrofolate-dehydrogenase-methenyltetrahydrofolate-cyclohydrolase
#6
Minhye Shin, Jessica Momb, Dean R Appling
Background: Folate-dependent one-carbon metabolism provides one-carbon units for several biological processes. This pathway is highly compartmentalized in eukaryotes, with the mitochondrial pathway producing formate for use in cytoplasmic processes. The mitochondrial enzyme MTHFD2 has been reported to use NAD+ as a cofactor while the isozyme MTHFD2L utilizes NAD+ or NADP+ at physiologically relevant conditions. Because MTHFD2 is highly expressed in many cancer types, we sought to determine the cofactor preference of this enzyme...
2017: Cancer & Metabolism
https://www.readbyqxmd.com/read/29214019/pkm2-is-not-required-for-colon-cancer-initiated-by-apc-loss
#7
Allison N Lau, William J Israelsen, Jatin Roper, Mark J Sinnamon, Larissa Georgeon, Talya L Dayton, Alissandra L Hillis, Omer H Yilmaz, Dolores Di Vizio, Kenneth E Hung, Matthew G Vander Heiden
Background: Cancer cells express the M2 isoform of the glycolytic enzyme pyruvate kinase (PKM2). PKM2 expression is not required for some cancers, and PKM2 loss can promote cancer progression; however, PKM2 has been reported to be essential in other tumor contexts, including a proposed non-metabolic role in β-catenin nuclear translocation. PKM2 is expressed in colon cancers where loss of the Apc tumor suppressor results in β-catenin nuclear translocation and aberrant activation of the canonical Wnt signaling pathway...
2017: Cancer & Metabolism
https://www.readbyqxmd.com/read/29093815/metabolomics-guided-pathway-analysis-reveals-link-between-cancer-metastasis-cholesterol-sulfate-and-phospholipids
#8
Caroline H Johnson, Antonio F Santidrian, Sarah E LeBoeuf, Michael E Kurczy, Nicholas J W Rattray, Zahra Rattray, Benedikt Warth, Melissa Ritland, Linh T Hoang, Celine Loriot, Jason Higa, James E Hansen, Brunhilde H Felding, Gary Siuzdak
Background: Cancer cells that enter the metastatic cascade require traits that allow them to survive within the circulation and colonize distant organ sites. As disseminating cancer cells adapt to their changing microenvironments, they also modify their metabolism and metabolite production. Methods: A mouse xenograft model of spontaneous tumor metastasis was used to determine the metabolic rewiring that occurs between primary cancers and their metastases. An "autonomous" mass spectrometry-based untargeted metabolomic workflow with integrative metabolic pathway analysis revealed a number of differentially regulated metabolites in primary mammary fat pad (MFP) tumors compared to microdissected paired lung metastases...
2017: Cancer & Metabolism
https://www.readbyqxmd.com/read/29026541/molecular-features-that-predict-the-response-to-antimetabolite-chemotherapies
#9
Mahya Mehrmohamadi, Seong Ho Jeong, Jason W Locasale
BACKGROUND: Antimetabolite chemotherapeutic agents that target cellular metabolism are widely used in the clinic and are thought to exert their anti-cancer effects mainly through non-specific cytotoxic effects. However, patients vary dramatically with respect to treatment outcome, and the sources of heterogeneity remain largely unknown. METHODS: Here, we introduce a computational method for identifying gene expression signatures of response to chemotherapies and apply it to human tumors and cancer cell lines...
2017: Cancer & Metabolism
https://www.readbyqxmd.com/read/28855983/bortezomib-resistance-in-multiple-myeloma-is-associated-with-increased-serine-synthesis
#10
Esther A Zaal, Wei Wu, Gerrit Jansen, Sonja Zweegman, Jacqueline Cloos, Celia R Berkers
BACKGROUND: The proteasome inhibitor bortezomib (BTZ) is successfully applied in the treatment of multiple myeloma, but its efficacy is restricted by the wide-spread occurrence of resistance. Metabolic alterations play an important role in cancer development and aid in the cellular adaptation to pharmacologically changed environments. Metabolic changes could therefore play an essential role in the development of drug resistance. However, specific metabolic pathways that can be targeted to improve bortezomib therapy remain unidentified...
2017: Cancer & Metabolism
https://www.readbyqxmd.com/read/28852500/metabolic-profiling-of-triple-negative-breast-cancer-cells-reveals-metabolic-vulnerabilities
#11
Nathan J Lanning, Joshua P Castle, Simar J Singh, Andre N Leon, Elizabeth A Tovar, Amandeep Sanghera, Jeffrey P MacKeigan, Fabian V Filipp, Carrie R Graveel
BACKGROUND: Among breast cancers, the triple-negative breast cancer (TNBC) subtype has the worst prognosis with no approved targeted therapies and only standard chemotherapy as the backbone of systemic therapy. Unique metabolic changes in cancer progression provide innovative therapeutic opportunities. The receptor tyrosine kinases (RTKs) epidermal growth factor receptor (EGFR), and MET receptor are highly expressed in TNBC, making both promising therapeutic targets. RTK signaling profoundly alters cellular metabolism by increasing glucose consumption and subsequently diverting glucose carbon sources into metabolic pathways necessary to support the tumorigenesis...
2017: Cancer & Metabolism
https://www.readbyqxmd.com/read/28680592/hif-prolyl-hydroxylase-phd3-regulates-translational-machinery-and-glucose-metabolism-in-clear-cell-renal-cell-carcinoma
#12
Petra Miikkulainen, Heidi Högel, Krista Rantanen, Tomi Suomi, Petri Kouvonen, Laura L Elo, Panu M Jaakkola
BACKGROUND: A key feature of clear cell renal cell carcinoma (ccRCC) is the inactivation of the von Hippel-Lindau tumour suppressor protein (pVHL) that leads to the activation of hypoxia-inducible factor (HIF) pathway also in well-oxygenated conditions. Important regulator of HIF-α, prolyl hydroxylase PHD3, is expressed in high amounts in ccRCC. Although several functions and downstream targets for PHD3 in cancer have been suggested, the role of elevated PHD3 expression in ccRCC is not clear...
2017: Cancer & Metabolism
https://www.readbyqxmd.com/read/28261475/the-action-of-%C3%AE-hydroxybutyrate-on-the-growth-metabolism-and-global-histone-h3-acetylation-of-spontaneous-mouse-mammary-tumours-evidence-of-a-%C3%AE-hydroxybutyrate-paradox
#13
Loreta M Rodrigues, Santiago Uribe-Lewis, Basetti Madhu, Davina J Honess, Marion Stubbs, John R Griffiths
BACKGROUND: Ketone bodies have both metabolic and epigenetic roles in cancer. In several studies, they showed an anti-cancer effect via inhibition of histone deacetylases; however, other studies observed faster tumour growth. The related molecule butyrate also inhibits growth of some cancer cells and accelerates it in others. This "butyrate paradox" is thought to be due to butyrate mediating histone acetylation and thus inhibiting cell proliferation in cancers that preferentially utilise glucose (the Warburg effect); whereas in cells that oxidise butyrate as a fuel, it fails to reach inhibitory concentrations and can stimulate growth...
2017: Cancer & Metabolism
https://www.readbyqxmd.com/read/28184304/the-%C3%AE-ketoglutarate-dehydrogenase-complex-in-cancer-metabolic-plasticity
#14
REVIEW
Renaud Vatrinet, Giulia Leone, Monica De Luise, Giulia Girolimetti, Michele Vidone, Giuseppe Gasparre, Anna Maria Porcelli
Deregulated metabolism is a well-established hallmark of cancer. At the hub of various metabolic pathways deeply integrated within mitochondrial functions, the α-ketoglutarate dehydrogenase complex represents a major modulator of electron transport chain activity and tricarboxylic acid cycle (TCA) flux, and is a pivotal enzyme in the metabolic reprogramming following a cancer cell's change in bioenergetic requirements. By contributing to the control of α-ketoglutarate levels, dynamics, and oxidation state, the α-ketoglutarate dehydrogenase is also essential in modulating the epigenetic landscape of cancer cells...
2017: Cancer & Metabolism
https://www.readbyqxmd.com/read/28163917/mitochondrial-mutations-and-metabolic-adaptation-in-pancreatic-cancer
#15
Rae-Anne Hardie, Ellen van Dam, Mark Cowley, Ting-Li Han, Seher Balaban, Marina Pajic, Mark Pinese, Mary Iconomou, Robert F Shearer, Jessie McKenna, David Miller, Nicola Waddell, John V Pearson, Sean M Grimmond, Leonid Sazanov, Andrew V Biankin, Silas Villas-Boas, Andrew J Hoy, Nigel Turner, Darren N Saunders
BACKGROUND: Pancreatic cancer has a five-year survival rate of ~8%, with characteristic molecular heterogeneity and restricted treatment options. Targeting metabolism has emerged as a potentially effective therapeutic strategy for cancers such as pancreatic cancer, which are driven by genetic alterations that are not tractable drug targets. Although somatic mitochondrial genome (mtDNA) mutations have been observed in various tumors types, understanding of metabolic genotype-phenotype relationships is limited...
2017: Cancer & Metabolism
https://www.readbyqxmd.com/read/28101337/adipocyte-lipolysis-links-obesity-to-breast-cancer-growth-adipocyte-derived-fatty-acids-drive-breast-cancer-cell-proliferation-and-migration
#16
Seher Balaban, Robert F Shearer, Lisa S Lee, Michelle van Geldermalsen, Mark Schreuder, Harrison C Shtein, Rose Cairns, Kristen C Thomas, Daniel J Fazakerley, Thomas Grewal, Jeff Holst, Darren N Saunders, Andrew J Hoy
BACKGROUND: Obesity is associated with increased recurrence and reduced survival of breast cancer. Adipocytes constitute a significant component of breast tissue, yet their role in provisioning metabolic substrates to support breast cancer progression is poorly understood. RESULTS: Here, we show that co-culture of breast cancer cells with adipocytes revealed cancer cell-stimulated depletion of adipocyte triacylglycerol. Adipocyte-derived free fatty acids were transferred to breast cancer cells, driving fatty acid metabolism via increased CPT1A and electron transport chain complex protein levels, resulting in increased proliferation and migration...
2017: Cancer & Metabolism
https://www.readbyqxmd.com/read/27980733/the-role-of-tumor-metabolism-as-a-driver-of-prostate-cancer-progression-and-lethal-disease-results-from-a-nested-case-control-study
#17
Rachel S Kelly, Jennifer A Sinnott, Jennifer R Rider, Ericka M Ebot, Travis Gerke, Michaela Bowden, Andreas Pettersson, Massimo Loda, Howard D Sesso, Philip W Kantoff, Neil E Martin, Edward L Giovannucci, Svitlana Tyekucheva, Matthew Vander Heiden, Lorelei A Mucci
BACKGROUND: Understanding the biologic mechanisms underlying the development of lethal prostate cancer is critical for improved therapeutic and prevention strategies. In this study we explored the role of tumor metabolism in prostate cancer progression using mRNA expression profiling of seven metabolic pathways; fatty acid metabolism, glycolysis/gluconeogenesis, oxidative phosphorylation, pentose phosphate, purine metabolism, pyrimidine metabolism and the tricarboxylic acid cycle. METHODS: The study included 404 men with archival formalin-fixed, paraffin-embedded prostate tumor tissue from the prospective Health Professionals Follow-up Study and Physicians' Health Study...
2016: Cancer & Metabolism
https://www.readbyqxmd.com/read/27980732/weight-control-interventions-improve-therapeutic-efficacy-of-dacarbazine-in-melanoma-by-reversing-obesity-induced-drug-resistance
#18
Parmanand Malvi, Balkrishna Chaube, Shivendra Vikram Singh, Naoshad Mohammad, Vimal Pandey, Maleppillil Vavachan Vijayakumar, Revathy Meenatheril Radhakrishnan, Muralidharan Vanuopadath, Sudarslal Sadasivan Nair, Bipin Gopalakrishnan Nair, Manoj Kumar Bhat
BACKGROUND: Obesity-related cellular, metabolic, and molecular alterations have been shown to increase cancer risk and tumor progression and are associated with poorer therapeutic outcome in cancer patients. However, the impact of obesity and weight-control interventions on the therapeutic response in melanoma is poorly understood. METHODS: High fat diet (HFD)-induced obese mouse model was used in this study to evaluate the outcome of dacarbazine (DTIC) therapy in melanoma...
2016: Cancer & Metabolism
https://www.readbyqxmd.com/read/27777765/epithelial-mesenchymal-transition-induction-is-associated-with-augmented-glucose-uptake-and-lactate-production-in-pancreatic-ductal-adenocarcinoma
#19
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
https://www.readbyqxmd.com/read/27729975/lactate-pyruvate-transporter-mct-1-is-a-direct-wnt-target-that-confers-sensitivity-to-3-bromopyruvate-in-colon-cancer
#20
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
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