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Metabolic reprogramming

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https://www.readbyqxmd.com/read/29684791/the-role-of-promyelocytic-leukemia-protein-in-steatosis-associated-hepatic-tumors-related-to-chronic-hepatitis-b-virus-infection
#1
Yih-Lin Chung, Mei-Ling Wu
The persistence of hepatitis B surface antigen (HBsAg) is a risk factor for the development of steatosis-associated tumors in chronic hepatitis B virus (HBV) infection, yet little is known about the metabolic link with this factor. We correlated HBV-related pathogenesis in genetically engineered mice and human carriers with metabolic proteomics and lipogenic gene expression profiles. The immunohistochemistry showed that the promyelocytic leukemia protein (PML, a tumor suppressor involved in genome maintenance and fatty acid oxidation), being inversely influenced by the dynamic HBsAg levels from acute phase to seroclearance, appeared as a lipo-metabolic switch linking HBsAg-induced steatosis (lipogenesis) to HBsAg-lost fat-burning hepatocarcinogenesis (lipolysis)...
April 20, 2018: Translational Oncology
https://www.readbyqxmd.com/read/29681442/evidence-that-tlr4-is-not-a-receptor-for-saturated-fatty-acids-but-mediates-lipid-induced-inflammation-by-reprogramming-macrophage-metabolism
#2
Graeme I Lancaster, Katherine G Langley, Nils Anton Berglund, Helene L Kammoun, Saskia Reibe, Emma Estevez, Jacquelyn Weir, Natalie A Mellett, Gerard Pernes, James R W Conway, Man K S Lee, Paul Timpson, Andrew J Murphy, Seth L Masters, Steve Gerondakis, Nenad Bartonicek, Dominik C Kaczorowski, Marcel E Dinger, Peter J Meikle, Peter J Bond, Mark A Febbraio
Chronic inflammation is a hallmark of obesity and is linked to the development of numerous diseases. The activation of toll-like receptor 4 (TLR4) by long-chain saturated fatty acids (lcSFAs) is an important process in understanding how obesity initiates inflammation. While experimental evidence supports an important role for TLR4 in obesity-induced inflammation in vivo, via a mechanism thought to involve direct binding to and activation of TLR4 by lcSFAs, several lines of evidence argue against lcSFAs being direct TLR4 agonists...
April 13, 2018: Cell Metabolism
https://www.readbyqxmd.com/read/29678957/a-new-role-for-extracellular-vesicles-how-small-vesicles-can-feed-tumors-big-appetite
#3
Ikrame Lazar, Emily Clement, Camille Attane, Catherine Muller, Laurence Nieto
Cancer cells must adapt their metabolism in order to meet the energy requirements for cell proliferation, survival in nutrient-deprived environments and dissemination. In particular, fatty acid metabolism is emerging as a critical process for tumors. Fatty acid metabolism can be modulated through intrinsic changes in gene expression or signaling between tumor cells, but also in response to signals from the surrounding microenvironment. Among these signals, extracellular vesicles could play an important role in fatty acid metabolism remodeling...
April 20, 2018: Journal of Lipid Research
https://www.readbyqxmd.com/read/29675460/epigenetic-reprogramming-of-human-hepatoma-cells-a-low-cost-option-for-drug-metabolism-assessment
#4
Luc Gailhouste, Lee Chuen Liew, Ken Yasukawa, Keitaro Hagiwara, Norihiko Iwazaki, Yasuhiro Yamada, Izuho Hatada, Takahiro Ochiya
No abstract text is available yet for this article.
March 2018: Cellular and Molecular Gastroenterology and Hepatology
https://www.readbyqxmd.com/read/29675398/metabolic-reprogramming-during-multidrug-resistance-in-leukemias
#5
Raphael Silveira Vidal, Julia Quarti, Franklin D Rumjanek, Vivian M Rumjanek
Cancer outcome has improved since introduction of target therapy. However, treatment success is still impaired by the same drug resistance mechanism of classical chemotherapy, known as multidrug resistance (MDR) phenotype. This phenotype promotes resistance to drugs with different structures and mechanism of action. Recent reports have shown that resistance acquisition is coupled to metabolic reprogramming. High-gene expression, increase of active transport, and conservation of redox status are one of the few examples that increase energy and substrate demands...
2018: Frontiers in Oncology
https://www.readbyqxmd.com/read/29675017/-de-novo-fatty-acid-synthesis-during-mycobacterial-infection-is-a-prerequisite-for-the-function-of-highly-proliferative-t-cells-but-not-for-dendritic-cells-or-macrophages
#6
Philipp Stüve, Lucía Minarrieta, Hanna Erdmann, Catharina Arnold-Schrauf, Maxine Swallow, Melanie Guderian, Freyja Krull, Alexandra Hölscher, Peyman Ghorbani, Jochen Behrends, Wolf-Rainer Abraham, Christoph Hölscher, Tim D Sparwasser, Luciana Berod
Mycobacterium tuberculosis ( Mtb ), the causative agent of human tuberculosis, is able to efficiently manipulate the host immune system establishing chronic infection, yet the underlying mechanisms of immune evasion are not fully understood. Evidence suggests that this pathogen interferes with host cell lipid metabolism to ensure its persistence. Fatty acid metabolism is regulated by acetyl-CoA carboxylase (ACC) 1 and 2; both isoforms catalyze the conversion of acetyl-CoA into malonyl-CoA, but have distinct roles...
2018: Frontiers in Immunology
https://www.readbyqxmd.com/read/29674963/a-bivalent-securinine-compound-sn3-l6-induces-neuronal-differentiation-via-translational-upregulation-of-neurogenic-transcription-factors
#7
Yumei Liao, Xiaoji Zhuang, Xiaojie Huang, Yinghui Peng, Xuanyue Ma, Zhi-Xing Huang, Feng Liu, Junyu Xu, Ying Wang, Wei-Min Chen, Wen-Cai Ye, Lei Shi
Developing therapeutic approaches that target neuronal differentiation will be greatly beneficial for the regeneration of neurons and synaptic networks in neurological diseases. Protein synthesis (mRNA translation) has recently been shown to regulate neurogenesis of neural stem/progenitor cells (NSPCs). However, it has remained unknown whether engineering translational machinery is a valid approach for manipulating neuronal differentiation. The present study identifies that a bivalent securinine compound SN3-L6, previously designed and synthesized by our group, induces potent neuronal differentiation through a novel translation-dependent mechanism...
2018: Frontiers in Pharmacology
https://www.readbyqxmd.com/read/29674282/bioenergetics-mechanisms-regulating-muscle-stem-cell-self-renewal-commitment-and-function
#8
REVIEW
Phablo Abreu
Muscle stem cells or satellite cells are crucial for muscle maintenance and repair. These cells are mitotically quiescent and uniformly express the transcription factor Pax7, intermittently entering the cell cycle to give rise to daughter myogenic precursors cells and fuse with neighboring myofibers or self-renew, replenishing the stem cell pool in adult skeletal muscle. Pivotal roles of muscle stem cells in muscle repair have been uncovered, but it still remains unclear how muscle stem cell self-renewal is molecularly regulated and how muscle stem cells maintain muscle tissue homeostasis...
April 16, 2018: Biomedicine & Pharmacotherapy, Biomédecine & Pharmacothérapie
https://www.readbyqxmd.com/read/29672864/menin-regulates-the-serine-biosynthetic-pathway-in-ewing-sarcoma
#9
Laurie K Svoboda, Selina Shiqing K Teh, Sudha Sud, Samuel Kerk, Aaron Zebolsky, Sydney Treichel, Dafydd Thomas, Christopher J Halbrook, Ho-Joon Lee, Daniel Kremer, Li Zhang, Szymon Klossowski, Armand R Bankhead, Brian Magnuson, Mats Ljungman, Tomasz Cierpicki, Jolanta Grembecka, Costas A Lyssiotis, Elizabeth R Lawlor
Developmental transcription programs are epigenetically regulated by multi-protein complexes, including the menin- and MLL-containing trithorax (TrxG) complexes, which promote gene transcription by depositing the H3K4me3 activating mark at target gene promoters. We recently reported that in Ewing sarcoma, MLL1 (lysine methyltransferase 2A, KMT2A) and menin are overexpressed and function as oncogenes. Small molecule inhibition of the menin-MLL interaction leads to loss of menin and MLL1 protein expression and to inhibition of growth and tumorigenicity...
April 19, 2018: Journal of Pathology
https://www.readbyqxmd.com/read/29670683/nrf2-mediated-metabolic-reprogramming-in-cancer
#10
REVIEW
Yan-Yang Wang, Juan Chen, Xiao-Ming Liu, Ren Zhao, Hong Zhe
Metabolic reprogramming is one of the hallmarks of cancer. Nrf2 pathway is one of the critical signaling cascades involved in cell defense and survival against oxidative stress. The significance of Nrf2 in cancer metabolism begins to be recognized. In this minireview, we focus on the Nrf2-mediated cancer metabolic reprogramming and intend to highlight the role of Nrf2 in the regulation of malignant transformation, cancer proliferation, and the development of treatment resistance via metabolic adaptations. We hope for the development of noninvasive biomarkers and novel therapeutic approaches for cancer based on Nrf2-directed cancer metabolic reprogramming in the near future...
2018: Oxidative Medicine and Cellular Longevity
https://www.readbyqxmd.com/read/29670296/paracrine-roles-of-cellular-senescence-in-promoting-tumourigenesis
#11
REVIEW
Jose Mario Gonzalez-Meljem, John Richard Apps, Helen Christina Fraser, Juan Pedro Martinez-Barbera
Senescent cells activate genetic programmes that irreversibly inhibit cellular proliferation, but also endow these cells with distinctive metabolic and signalling phenotypes. Although senescence has historically been considered a protective mechanism against tumourigenesis, the activities of senescent cells are increasingly being associated with age-related diseases, including cancer. An important feature of senescent cells is the secretion of a vast array of pro-inflammatory cytokines, chemokines, and growth factors collectively known as the senescence-associated secretory phenotype (SASP)...
April 19, 2018: British Journal of Cancer
https://www.readbyqxmd.com/read/29669277/modulation-of-tau-isoforms-imbalance-precludes-tau-pathology-and-cognitive-decline-in-a-mouse-model-of-tauopathy
#12
Sonia Lorena Espíndola, Ana Damianich, Rodrigo Javier Alvarez, Manuela Sartor, Juan Emilio Belforte, Juan Esteban Ferrario, Jean-Marc Gallo, María Elena Avale
The microtubule-associated protein tau regulates myriad neuronal functions, such as microtubule dynamics, axonal transport and neurite outgrowth. Tauopathies are neurodegenerative disorders characterized by the abnormal metabolism of tau, which accumulates as insoluble neuronal deposits. The adult human brain contains equal amounts of tau isoforms with three (3R) or four (4R) repeats of microtubule-binding domains, derived from the alternative splicing of exon 10 (E10) in the tau transcript. Several tauopathies are associated with imbalances of tau isoforms, due to splicing deficits...
April 17, 2018: Cell Reports
https://www.readbyqxmd.com/read/29666451/exploring-the-extent-and-scope-of-epigenetic-inheritance
#13
REVIEW
Elizabeth J Radford
Environmental factors, particularly during early life, are important for the later metabolic health of the individual. In our obesogenic environment, it is of major socio-economic importance to investigate the mechanisms that contribute to the risk of metabolic ill health. Increasing evidence from a variety of model organisms suggests that non-genetically determined phenotypes, including metabolic effects such as glucose intolerance and obesity, can be passed between generations, which encourages us to revisit heredity...
April 17, 2018: Nature Reviews. Endocrinology
https://www.readbyqxmd.com/read/29666362/cooperative-stat-nf-%C3%AE%C2%BAb-signaling-regulates-lymphoma-metabolic-reprogramming-and-aberrant-got2-expression
#14
Maren Feist, Philipp Schwarzfischer, Paul Heinrich, Xueni Sun, Judith Kemper, Frederike von Bonin, Paula Perez-Rubio, Franziska Taruttis, Thorsten Rehberg, Katja Dettmer, Wolfram Gronwald, Jörg Reinders, Julia C Engelmann, Jan Dudek, Wolfram Klapper, Lorenz Trümper, Rainer Spang, Peter J Oefner, Dieter Kube
Knowledge of stromal factors that have a role in the transcriptional regulation of metabolic pathways aside from c-Myc is fundamental to improvements in lymphoma therapy. Using a MYC-inducible human B-cell line, we observed the cooperative activation of STAT3 and NF-κB by IL10 and CpG stimulation. We show that IL10 + CpG-mediated cell proliferation of MYClow cells depends on glutaminolysis. By 13 C- and 15 N-tracing of glutamine metabolism and metabolite rescue experiments, we demonstrate that GOT2 provides aspartate and nucleotides to cells with activated or aberrant Jak/STAT and NF-κB signaling...
April 17, 2018: Nature Communications
https://www.readbyqxmd.com/read/29665673/cooperative-instruction-of-signaling-and-metabolic-pathways-on-the-epigenetic-landscape
#15
Jung-Ae Kim
Cells cope with diverse intrinsic and extrinsic stimuli in order to make adaptations for survival. The epigenetic landscape plays a crucial role in cellular adaptation, as it integrates the information generated from stimuli. Signaling pathways induced by stimuli communicate with chromatin to change the epigenetic landscape through regulation of epigenetic modifiers. Metabolic dynamics altered by these stimuli also affect the activity of epigenetic modifiers. Here, I review the current understanding of epigenetic regulation via signaling and metabolic pathways...
April 11, 2018: Molecules and Cells
https://www.readbyqxmd.com/read/29663393/maternal-obesity-reprograms-offspring-s-executive-brain-centers-in-a-sex-specific-manner-an-editorial-for-perinatal-high-fat-diet-and-early-life-methyl-donor-supplementation-alter-one-carbon-metabolism-and-dna-methylation-in-the-brain-on-doi-10-1111-jnc-14319
#16
EDITORIAL
Kaja Plucińska, Steven W Barger
This editorial highlights an article by McKee and colleagues in the current issue of Journal of Neurochemistry, in which the authors report epigenetic changes linked to one-carbon metabolism in prefrontal cortex (PFC) of murine offspring from dams fed high-fat diet to mimic maternal obesity. The group found that high-fat diet feeding in utero increases weight gain in offspring and dynamically alters DNA methylation in the PFC of male but not female brains. These epigenetic marks were associated with a shift in brain one-carbon metabolism (folate and methionine) intermediates and were normalized by early-life methyl-donor supplementation in a sex-specific manner...
April 16, 2018: Journal of Neurochemistry
https://www.readbyqxmd.com/read/29662176/cancer-cell-secreted-exosomal-mir-105-promotes-tumour-growth-through-the-myc-dependent-metabolic-reprogramming-of-stromal-cells
#17
Wei Yan, Xiwei Wu, Weiying Zhou, Miranda Y Fong, Minghui Cao, Juan Liu, Xiaojing Liu, Chih-Hong Chen, Oluwole Fadare, Donald P Pizzo, Jiawen Wu, Liang Liu, Xuxiang Liu, Andrew R Chin, Xiubao Ren, Yuan Chen, Jason W Locasale, Shizhen Emily Wang
Cancer and other cells residing in the same niche engage various modes of interactions to synchronize and buffer the negative effects of environmental changes. Extracellular microRNAs (miRNAs) have recently been implicated in the intercellular crosstalk. Here we show a mechanistic model involving breast-cancer-secreted, extracellular-vesicle-encapsulated miR-105, which is induced by the oncoprotein MYC in cancer cells and, in turn, activates MYC signalling in cancer-associated fibroblasts (CAFs) to induce a metabolic program...
April 16, 2018: Nature Cell Biology
https://www.readbyqxmd.com/read/29662084/hoxa9-inhibits-hif-1%C3%AE-mediated-glycolysis-through-interacting-with-crip2-to-repress-cutaneous-squamous-cell-carcinoma-development
#18
Liang Zhou, Yinghui Wang, Meijuan Zhou, Ying Zhang, Pengfei Wang, Xiaoxing Li, Jing Yang, Hongmei Wang, Zhenhua Ding
Glycolytic reprogramming is a typical feature of many cancers; however, key regulators of glucose metabolism reengineering are poorly understood, especially in cutaneous squamous cell carcinoma (cSCC). Here, Homeobox A9 (HOXA9), a direct target of onco-miR-365, is identified to be significantly downregulated in cSCC tumors and cell lines. HOXA9 acts as a tumor suppressor and inhibits glycolysis in cSCC in vitro and in vivo by negatively regulating HIF-1α and its downstream glycolytic regulators, HK2, GLUT1 and PDK1...
April 16, 2018: Nature Communications
https://www.readbyqxmd.com/read/29662077/pharmacodynamics-of-mutant-idh1-inhibitors-in-glioma-patients-probed-by-in-vivo-3d-mrs-imaging-of-2-hydroxyglutarate
#19
Ovidiu C Andronesi, Isabel C Arrillaga-Romany, K Ina Ly, Wolfgang Bogner, Eva M Ratai, Kara Reitz, A John Iafrate, Jorg Dietrich, Elizabeth R Gerstner, Andrew S Chi, Bruce R Rosen, Patrick Y Wen, Daniel P Cahill, Tracy T Batchelor
Inhibitors of the mutant isocitrate dehydrogenase 1 (IDH1) entered recently in clinical trials for glioma treatment. Mutant IDH1 produces high levels of 2-hydroxyglurate (2HG), thought to initiate oncogenesis through epigenetic modifications of gene expression. In this study, we show the initial evidence of the pharmacodynamics of a new mutant IDH1 inhibitor in glioma patients, using non-invasive 3D MR spectroscopic imaging of 2HG. Our results from a Phase 1 clinical trial indicate a rapid decrease of 2HG levels by 70% (CI 13%, P = 0...
April 16, 2018: Nature Communications
https://www.readbyqxmd.com/read/29661856/glutamine-utilizing-transaminases-are-a-metabolic-vulnerability-of-taz-yap-activated-cancer-cells
#20
Chih-Sheng Yang, Eleni Stampouloglou, Nathan M Kingston, Liye Zhang, Stefano Monti, Xaralabos Varelas
The transcriptional regulators TAZ and YAP (TAZ/YAP) have emerged as pro-tumorigenic factors that drive many oncogenic traits, including induction of cell growth, resistance to cell death, and activation of processes that promote migration and invasion. Here, we report that TAZ/YAP reprogram cellular energetics to promote the dependence of breast cancer cell growth on exogenous glutamine. Rescue experiments with glutamine-derived metabolites suggest an essential role for glutamate and α-ketoglutarate (AKG) in TAZ/YAP-driven cell growth in the absence of glutamine...
April 16, 2018: EMBO Reports
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