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Metabolic reprogramming

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https://www.readbyqxmd.com/read/28725231/chloroplast-redox-status-modulates-genome-wide-plant-responses-during-the-non-host-interaction-of-tobacco-with-the-hemibiotrophic-bacterium-xanthomonas-campestris-pv-vesicatoria
#1
Juan J Pierella Karlusich, Matias D Zurbriggen, Fahimeh Shahinnia, Sophia Sonnewald, Uwe Sonnewald, Seyed A Hosseini, Mohammad-Reza Hajirezaei, Néstor Carrillo
Non-host resistance is the most ample and durable form of plant resistance against pathogen infection. It includes induction of defense-associated genes, massive metabolic reprogramming, and in many instances, a form of localized cell death (LCD) at the site of infection, purportedly designed to limit the spread of biotrophic and hemibiotrophic microorganisms. Reactive oxygen species (ROS) have been proposed to act as signals for LCD orchestration. They are produced in various cellular compartments including chloroplasts, mitochondria and apoplast...
2017: Frontiers in Plant Science
https://www.readbyqxmd.com/read/28724614/nuclear-mtor-acts-as-a-transcriptional-integrator-of-the-androgen-signaling-pathway-in-prostate-cancer
#2
Étienne Audet-Walsh, Catherine R Dufour, Tracey Yee, Fatima Z Zouanat, Ming Yan, Georges Kalloghlian, Mathieu Vernier, Maxime Caron, Guillaume Bourque, Eleonora Scarlata, Lucie Hamel, Fadi Brimo, Armen G Aprikian, Jacques Lapointe, Simone Chevalier, Vincent Giguère
Androgen receptor (AR) signaling reprograms cellular metabolism to support prostate cancer (PCa) growth and survival. Another key regulator of cellular metabolism is mTOR, a kinase found in diverse protein complexes and cellular localizations, including the nucleus. However, whether nuclear mTOR plays a role in PCa progression and participates in direct transcriptional cross-talk with the AR is unknown. Here, via the intersection of gene expression, genomic, and metabolic studies, we reveal the existence of a nuclear mTOR-AR transcriptional axis integral to the metabolic rewiring of PCa cells...
July 19, 2017: Genes & Development
https://www.readbyqxmd.com/read/28723673/energy-metabolism-in-glioblastoma-stem-cells-ppar%C3%AE-a-metabolic-adaptor-to-intratumoral-microenvironment
#3
Alessia Fidoamore, Loredana Cristiano, Chiara Laezza, Renato Galzio, Elisabetta Benedetti, Benedetta Cinque, Andrea Antonosante, Michele d'Angelo, Vanessa Castelli, Maria Grazia Cifone, Rodolfo Ippoliti, Antonio Giordano, Annamaria Cimini
Glioblastoma (GB), the most-common cancer in the adult brain, despite surgery and radio/ chemotherapy, is to date almost incurable. Many hypoxic tumors, including GB, show metabolic reprogramming to sustain uncontrolled proliferation, hypoxic conditions and angiogenesis. Peroxisome Proliferator-activated Receptors (PPAR), particularly the α isotype, have been involved in the control of energetic metabolism. Herein, we characterized patient-derived GB neurospheres focusing on their energetic metabolism and PPARα expression...
July 7, 2017: Oncotarget
https://www.readbyqxmd.com/read/28723563/a-positive-feedback-loop-between-sestrin2-and-mtorc2-is-required-for-the-survival-of-glutamine-depleted-lung-cancer-cells
#4
Jun-Kyu Byun, Yeon-Kyung Choi, Ji-Hyun Kim, Ji Yun Jeong, Hui-Jeon Jeon, Mi-Kyung Kim, Ilseon Hwang, Shin-Yup Lee, You Mie Lee, In-Kyu Lee, Keun-Gyu Park
Proper regulation of mTORC1 and mTORC2 upon nutrient starvation is critical for cancer cell survival. Upregulation of Sestrin2 in response to glutamine deprivation rescues cell death by suppressing mTORC1. However, the contribution of mTORC2 to Sestrin2-mediated mTORC1 suppression remains unclear. Here, we report that both Sestrin2 and mTORC2 are upregulated in glutamine-depleted lung cancer cells. Moreover, glutamine depletion caused Sestrin2 to associate with mTORC2, which was required for the increase in Sestrin2 protein stability and the reduction in mTORC1 activity...
July 18, 2017: Cell Reports
https://www.readbyqxmd.com/read/28722313/cellular-glycosylation-senses-metabolic-changes-and-modulates-cell-plasticity-during-emt
#5
REVIEW
P Carvalho-Cruz, F Alisson-Silva, A R Todeschini, W B Dias
Epithelial to mesenchymal transition (EMT) is a developmental program reactivated by tumor cells that leads to the switch from epithelial to mesenchymal phenotype. During EMT, cells are transcriptionally regulated to decrease E-cadherin expression while expressing mesenchymal markers such as vimentin, fibronectin and N-cadherin. Growing body of evidences suggest that cells engaged in EMT undergo a metabolic reprograming process, redirecting glucose flux toward Hexosamine Biosynthesis Pathway (HBP) which fuels aberrant glycosylation patterns that are extensively observed in cancer cells...
July 19, 2017: Developmental Dynamics: An Official Publication of the American Association of Anatomists
https://www.readbyqxmd.com/read/28720669/muc1-mediated-metabolic-alterations-regulate-response-to-radiotherapy-in-pancreatic-cancer
#6
Venugopal Gunda, Joshua J Souchek, Jaime Abrego, Surendra K Shukla, Gennifer D Goode, Enza Vernucci, Aneesha Dasgupta, Nina CHaika, Ryan J King, Sicong Li, Shuo Wang, Fang Yu, Tadayoshi Bessho, Chi Lin, Pankaj K Singh
Purpose: MUC1, an oncogene overexpressed in multiple solid tumors including pancreatic cancer, reduces overall survival and imparts resistance to radiation and chemotherapies. We previously identified that MUC1 facilitates growth promoting metabolic alterations in pancreatic cancer cells. The present study investigates the role of MUC1-mediated metabolism in radiation resistance of pancreatic cancer by utilizing cell lines and in vivo models. <p>Experimental design: We used MUC1 knockdown and overexpressed cell line models for evaluating the role of MUC1-mediated metabolism in radiation resistance through in vitro cytotoxicity, clonogenicity, DNA damage response and metabolomic evaluations...
July 18, 2017: Clinical Cancer Research: An Official Journal of the American Association for Cancer Research
https://www.readbyqxmd.com/read/28720588/ews-fli-is-a-master-regulator-of-metabolic-reprogramming-in-ewing-sarcoma
#7
Jason M Tanner, Claire Bensard, Peng Wei, Nathan M Krah, John C Schell, Jamie D Gardiner, Joshua D Schiffman, Stephen L Lessnick, Jared Rutter
Ewing sarcoma is a bone malignancy driven by a translocation event resulting in the fusion protein EWS/FLI1 (EF). EF functions as an aberrant and oncogenic transcription factor that misregulates the expression of thousands of genes. Previous work has focused principally on determining important transcriptional targets of EF, as well as characterizing important regulatory partnerships in EF-dependent transcriptional programs. Less is known, however, about EF-dependent metabolic changes or their role in Ewing sarcoma biology...
July 18, 2017: Molecular Cancer Research: MCR
https://www.readbyqxmd.com/read/28716939/distinct-requirements-for-energy-metabolism-in-mouse-primordial-germ-cells-and-their-reprogramming-to-embryonic-germ-cells
#8
Yohei Hayashi, Kei Otsuka, Masayuki Ebina, Kaori Igarashi, Asuka Takehara, Mitsuyo Matsumoto, Akio Kanai, Kazuhiko Igarashi, Tomoyoshi Soga, Yasuhisa Matsui
Primordial germ cells (PGCs), undifferentiated embryonic germ cells, are the only cells that have the ability to become gametes and to reacquire totipotency upon fertilization. It is generally understood that the development of PGCs proceeds through the expression of germ cell-specific transcription factors and characteristic epigenomic changes. However, little is known about the properties of PGCs at the metabolite and protein levels, which are directly responsible for the control of cell function. Here, we report the distinct energy metabolism of PGCs compared with that of embryonic stem cells...
July 17, 2017: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/28715126/an-engineered-photoswitchable-mammalian-pyruvate-kinase
#9
Stefanie Gehrig, Jamie A Macpherson, Paul C Driscoll, Alastair Symon, Stephen R Martin, James I MacRae, Jens Kleinjung, Franca Fraternali, Dimitrios Anastasiou
Changes in allosteric regulation of glycolytic enzymes have been linked to metabolic reprogramming involved in cancer. Remarkably, allosteric mechanisms control enzyme function at significantly shorter time-scales compared to the long-term effects of metabolic reprogramming on cell proliferation. It remains unclear if and how the speed and reversibility afforded by rapid allosteric control of metabolic enzymes is important for cell proliferation. Tools that allow specific, dynamic modulation of enzymatic activities in mammalian cells would help address this question...
July 17, 2017: FEBS Journal
https://www.readbyqxmd.com/read/28714978/%C3%AE-ketoglutarate-orchestrates-macrophage-activation-through-metabolic-and-epigenetic-reprogramming
#10
Pu-Ste Liu, Haiping Wang, Xiaoyun Li, Tung Chao, Tony Teav, Stefan Christen, Giusy Di Conza, Wan-Chen Cheng, Chih-Hung Chou, Magdalena Vavakova, Charlotte Muret, Koen Debackere, Massimiliano Mazzone, Hsien-Da Huang, Sarah-Maria Fendt, Julijana Ivanisevic, Ping-Chih Ho
Glutamine metabolism provides synergistic support for macrophage activation and elicitation of desirable immune responses; however, the underlying mechanisms regulated by glutamine metabolism to orchestrate macrophage activation remain unclear. Here we show that the production of α-ketoglutarate (αKG) via glutaminolysis is important for alternative (M2) activation of macrophages, including engagement of fatty acid oxidation (FAO) and Jmjd3-dependent epigenetic reprogramming of M2 genes. This M2-promoting mechanism is further modulated by a high αKG/succinate ratio, whereas a low ratio strengthens the proinflammatory phenotype in classically activated (M1) macrophages...
July 17, 2017: Nature Immunology
https://www.readbyqxmd.com/read/28714135/yap-suppresses-gluconeogenic-gene-expression-via-pgc1%C3%AE
#11
Yue Hu, Dong-Ju Shin, Hui Pan, Zhiqiang Lin, Jonathan M Dreyfuss, Fernando D Camargo, Ji Miao, Sudha B Biddinger
Cell growth and proliferation are tightly coupled to metabolism, and dissecting the signaling molecules which link these processes is an important step towards understanding development, regeneration and cancer. The transcriptional regulator Yes-associated protein 1 (YAP) is a key regulator of liver size, development and function. We now show that YAP can also suppress gluconeogenic gene expression. Yap deletion in primary hepatocytes potentiates the gluconeogenic gene response to glucagon and dexamethasone, whereas constitutively active YAP suppresses it...
July 17, 2017: Hepatology: Official Journal of the American Association for the Study of Liver Diseases
https://www.readbyqxmd.com/read/28711923/acute-myeloid-leukemia-cells-require-6-phosphogluconate-dehydrogenase-for-cell-growth-and-nadph-dependent-metabolic-reprogramming
#12
Haymanti Bhanot, Ellen L Weisberg, Mamatha M Reddy, Atsushi Nonami, Donna Neuberg, Richard M Stone, Klaus Podar, Ravi Salgia, James D Griffin, Martin Sattler
Acute myeloid leukemia (AML) cells are highly dependent on glycolytic pathways to generate metabolic energy and support cell growth, hinting at specific, targetable vulnerabilities as potential novel targets for drug development. Elevated levels of NADPH, a central metabolic factor involved in redox reactions, are common in myeloid leukemia cells, but the significance or biochemical basis underlying this increase is unknown. Using a small molecule analog that efficiently inhibits NADPH-producing enzymes, we found that AML cells require NADPH homeostasis for cell growth...
June 28, 2017: Oncotarget
https://www.readbyqxmd.com/read/28710412/exosomes-derived-from-pancreatic-cancer-cells-induce-insulin-resistance-in-c2c12-myotube-cells-through-the-pi3k-akt-foxo1-pathway
#13
Lantian Wang, Bo Zhang, Wen Zheng, Muxing Kang, Qing Chen, Wenjie Qin, Chao Li, Yuefeng Zhang, Yingkuan Shao, Yulian Wu
Prospective epidemiological studies have consistently suggested that pancreatic cancer-associated new-onset diabetes mellitus (PC-DM) represents a potential platform for early diagnose of pancreatic cancer (PC). Despite the studies performed, the mechanism behind this phenomenon remains ambiguous. In this study, we explored the effects of two types of exosomes released by murine pancreatic cancer and ductal epithelial cells on murine skeletal muscle cells. The results show that PC-derived exosomes can readily enter C2C12 myotubes, triggering lipidosis and glucose intake inhibition...
July 14, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28710132/autophagy-deficiency-compromises-alternative-pathways-of-respiration-following-energy-deprivation
#14
Jessica As Barros, João Henrique F Cavalcanti, David B Medeiros, Adriano Nunes-Nesi, Tamar Avin-Wittenberg, Alisdair R Fernie, Wagner Araujo
Under heterotrophic conditions carbohydrate oxidation inside the mitochondria is the primary energy source for cellular metabolism. However, during energy-limited conditions, alternative substrates are required to support respiration. Amino acid oxidation in plant cells plays a key role in this by generating electrons that can be transferred to the mitochondrial electron transport chain via the electron transfer flavoprotein/ubiquinone oxidoreductase system. Autophagy, a catabolic mechanism for macromolecule and protein recycling, allows the maintenance of amino acid pools and nutrient remobilization...
July 14, 2017: Plant Physiology
https://www.readbyqxmd.com/read/28707979/emerging-roles-for-sirt5-in-metabolism-and-cancer
#15
Lauren Rose Bringman-Rodenbarger, Angela H Guo, Costas A Lyssiotis, David B Lombard
SIGNIFICANCE: Developing evidence in the literature suggests that SIRT5 may be involved in metabolic reprogramming, an emerging hallmark of cancer by which neoplastic cells reconfigure their metabolism to support the anabolic demands of rapid cell division. Sirtuin 5 (SIRT5) is one of the seven members of the nicotinamide adenine dinucleotide (NAD+)-dependent sirtuin family of lysine deacylases. It removes succinyl, malonyl, and glutaryl groups from protein targets within the mitochondrial matrix and other subcellular compartments...
July 14, 2017: Antioxidants & Redox Signaling
https://www.readbyqxmd.com/read/28704618/paracoccidioides-brasiliensis-presents-metabolic-reprogramming-and-secretes-a-serine-proteinase-during-murine-infection
#16
Laurine Lacerda Pigosso, Lilian Cristiane Baeza, Mariana Vieira Tomazett, Mariana Batista Rodrigues Faleiro, Veridiana Maria Brianezi Dignani de Moura, Alexandre Melo Bailão, Clayton Luiz Borges, Juliana Alves Parente Rocha, Gabriel Rocha Fernandes, Gregory M Gauthier, Celia Maria de Almeida Soares
Paracoccidoides brasiliensis and Paracoccidioides lutzii, the etiologic agents of paracoccidioidomycosis, cause disease in healthy and immunocompromised persons in Latin America. We developed a method for harvesting P. brasiliensis yeast cells from infected murine lung to facilitate in vivo transcriptional and proteomic profiling. P. brasiliensis harvested at 6 h post-infection were analyzed using RNAseq and LC-MS(E). In vivo yeast cells had 594 differentially expressed transcripts and 350 differentially expressed proteins...
July 13, 2017: Virulence
https://www.readbyqxmd.com/read/28702319/grandpaternal-induced-transgenerational-dietary-reprogramming-of-the-unfolded-protein-response-in-skeletal-muscle
#17
Petter S Alm, Thais de Castro Barbosa, Romain Barrès, Anna Krook, Juleen R Zierath
OBJECTIVE: Parental nutrition and lifestyle impact the metabolic phenotype of the offspring. We have reported that grandpaternal chronic high-fat diet (HFD) transgenerationally impairs glucose metabolism in subsequent generations. Here we determined whether grandpaternal diet transgenerationally impacts the transcriptome and lipidome in skeletal muscle. Our aim was to identify tissue-specific pathways involved in transgenerational inheritance of environmental-induced phenotypes. METHODS: F0 male Sprague-Dawley rats were fed a HFD or chow for 12 weeks before breeding with chow-fed females to generate the F1 generation...
July 2017: Molecular Metabolism
https://www.readbyqxmd.com/read/28699638/bcat1-controls-metabolic-reprogramming-in-activated-human-macrophages-and-is-associated-with-inflammatory-diseases
#18
Adonia E Papathanassiu, Jeong-Hun Ko, Martha Imprialou, Marta Bagnati, Prashant K Srivastava, Hong A Vu, Danilo Cucchi, Stephen P McAdoo, Elitsa A Ananieva, Claudio Mauro, Jacques Behmoaras
Branched-chain aminotransferases (BCAT) are enzymes that initiate the catabolism of branched-chain amino acids (BCAA), such as leucine, thereby providing macromolecule precursors; however, the function of BCATs in macrophages is unknown. Here we show that BCAT1 is the predominant BCAT isoform in human primary macrophages. We identify ERG240 as a leucine analogue that blocks BCAT1 activity. Selective inhibition of BCAT1 activity results in decreased oxygen consumption and glycolysis. This decrease is associated with reduced IRG1 levels and itaconate synthesis, suggesting involvement of BCAA catabolism through the IRG1/itaconate axis within the tricarboxylic acid cycle in activated macrophages...
July 12, 2017: Nature Communications
https://www.readbyqxmd.com/read/28698932/small-molecules-for-reprogramming-and-transdifferentiation
#19
REVIEW
Hua Qin, Andong Zhao, Xiaobing Fu
Pluripotency reprogramming and transdifferentiation induced by transcription factors can generate induced pluripotent stem cells, adult stem cells or specialized cells. However, the induction efficiency and the reintroduction of exogenous genes limit their translation into clinical applications. Small molecules that target signaling pathways, epigenetic modifications, or metabolic processes can regulate cell development, cell fate, and function. In the recent decade, small molecules have been widely used in reprogramming and transdifferentiation fields, which can promote the induction efficiency, replace exogenous genes, or even induce cell fate conversion alone...
July 11, 2017: Cellular and Molecular Life Sciences: CMLS
https://www.readbyqxmd.com/read/28698547/metabolic-reprogramming-is-associated-with-flavopiridol-resistance-in-prostate-cancer-du145-cells
#20
Xiaoran Li, Jie Lu, Quancheng Kan, Xiaoli Li, Qiong Fan, Yaqing Li, Ruixia Huang, Ana Slipicevic, Hiep Phuc Dong, Lars Eide, Junbai Wang, Hongquan Zhang, Viktor Berge, Mariusz Adam Goscinski, Gunnar Kvalheim, Jahn M Nesland, Zhenhe Suo
Flavopiridol (FP) is a pan-cyclin dependent kinase inhibitor, which shows strong efficacy in inducing cancer cell apoptosis. Although FP is potent against most cancer cells in vitro, unfortunately it proved less efficacious in clinical trials in various aggressive cancers. To date, the molecular mechanisms of the FP resistance are mostly unknown. Here, we report that a small fraction human prostate cancer DU145 cells can survive long-term FP treatment and emerge as FP-resistant cells (DU145(FP)). These DU145(FP) cells show accumulated mitochondrial lesions with stronger glycolytic features, and they proliferate in slow-cycling and behave highly migratory with strong anti-apoptotic potential...
July 11, 2017: Scientific Reports
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