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[PMID]:29337061
[Au] Autor:Li Q; Qin Z; Nie F; Bi H; Zhao R; Pan B; Ma J; Xie X
[Ad] Endereço:Department of Plastic and Reconstructive Surgery, Peking University Third Hospital, Beijing, 100191, China.
[Ti] Título:Metabolic reprogramming in keloid fibroblasts: Aerobic glycolysis and a novel therapeutic strategy.
[So] Source:Biochem Biophys Res Commun;496(2):641-647, 2018 02 05.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Keloids, tumor-like fibroproliferative cutaneous lesions, were reported in metabolic disturbance. However, the metabolic character remains unclear. The purpose of this study is to determine if glycolytic reprogramming is important for the pathogenesis of keloids and to assess the inhibition potential of glycolysis in keloid treatment. An intracellular metabolic profile assay was used to compare metabolic phenotypes between normal skin fibroblasts and keloid fibroblasts (NFs and KFs). Our data indicated that KFs underwent reprogramming of their metabolic phonotype from oxidative phosphorylation to aerobic glycolysis (Warburg effect) with augmented glycolysis and glycolytic capacity. Both gene and protein assays showed that the expression of glycolytic enzymes was upregulated in KFs compared to NFs. Our data showed higher glucose influx and lactate production in KFs compared to NFs. Furthermore, the proliferation of KFs was suppressed in a dose-dependent and time-dependent manner after inhibition of glycolysis with 2-deoxy-glucose (2-DG). Taken together, these findings suggested that keloids underwent a reprogrammed metabolic phenotype of aerobic glycolysis. This was essential for keloid hyperplasia, and glycolytic inhibitors might provide a potential treatment for keloids.
[Mh] Termos MeSH primário: Fibroblastos/patologia
Queloide/patologia
[Mh] Termos MeSH secundário: Proliferação Celular/efeitos dos fármacos
Células Cultivadas
Desoxiglucose/farmacologia
Fibroblastos/efeitos dos fármacos
Fibroblastos/metabolismo
Regulação da Expressão Gênica
Glucose/metabolismo
Glicólise/efeitos dos fármacos
Seres Humanos
Queloide/tratamento farmacológico
Queloide/genética
Queloide/metabolismo
Ácido Láctico/metabolismo
Consumo de Oxigênio
Pele/metabolismo
Pele/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
33X04XA5AT (Lactic Acid); 9G2MP84A8W (Deoxyglucose); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180117
[St] Status:MEDLINE


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[PMID]:29268130
[Au] Autor:Lin HY; Han HW; Sun WX; Yang YS; Tang CY; Lu GH; Qi JL; Wang XM; Yang YH
[Ad] Endereço:State Key Laboratory of Pharmaceutical Biotechnology, NJU-NJFU Institute of Plant Molecular Biology, School of Life Sciences, Nanjing University, Nanjing, 210023, China; Co-Innovation Center for Sustainable Forestry in Southern China, Nanjing Forestry University, Nanjing, 210037, China.
[Ti] Título:Design and characterization of α-lipoic acyl shikonin ester twin drugs as tubulin and PDK1 dual inhibitors.
[So] Source:Eur J Med Chem;144:137-150, 2018 Jan 20.
[Is] ISSN:1768-3254
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:Shikonin exhibits powerful anticancer activities for various cancer cells, but its poor solubility and strong toxicity hinder its development as clinical anticancer agent. We previously confirmed that shikonin and its derivatives can disturb mitosis through targeting tubulin. In this study, α-lipoic acid, the naturally-occurring co-factor of pyruvate dehydrogenase (PDH), was introduced into shikonin to design the twin drugs against both mitosis (tubulin) and glycolysis (PDK). 18 kinds of α-lipoic acid shikonin ester derivatives were achieved through three rounds of screening process performed by computer assistant drug design method, being designated as the outstanding compounds. Among them, 1c displayed the most potent cytotoxicity towards cervical cancer cells (HeLa) with an IC value of 3.14 ± 0.58 µM and inhibited xenotransplanted tumor growth in a dose-dependent manner. Further pharmacologic study demonstrated that 1c can cause cell cycle arrest in G2/M phase as tubulin polymerization inhibitor. Moreover, it also showed good PDK1 inhibitory activity, promoting PDH activity and forced HeLa cells to process more aerobic metabolism to undergo cell apoptosis. We reported here the first dual inhibitors of tubulin and PDK1 based on shikonin. It may form a basis for shikonin optimization through twin drug design framework for the discovery of new and potent shikonin derivatives in the study of targeted cancer therapy.
[Mh] Termos MeSH primário: Antineoplásicos/química
Antineoplásicos/farmacologia
Naftoquinonas/química
Naftoquinonas/farmacologia
Proteínas Serina-Treonina Quinases/antagonistas & inibidores
Moduladores de Tubulina/química
Moduladores de Tubulina/farmacologia
[Mh] Termos MeSH secundário: Apoptose/efeitos dos fármacos
Pontos de Checagem do Ciclo Celular/efeitos dos fármacos
Desenho de Drogas
Glicólise/efeitos dos fármacos
Células HeLa
Seres Humanos
Mitose/efeitos dos fármacos
Neoplasias/tratamento farmacológico
Neoplasias/metabolismo
Proteínas Serina-Treonina Quinases/metabolismo
Tubulina (Proteína)/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Naphthoquinones); 0 (Tubulin); 0 (Tubulin Modulators); 3IK6592UBW (shikonin); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); EC 2.7.11.2 (pyruvate dehydrogenase (acetyl-transferring) kinase)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171222
[St] Status:MEDLINE


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[PMID]:29202688
[Au] Autor:Abrahamian M; Kagda M; Ah-Fong AMV; Judelson HS
[Ad] Endereço:Department of Microbiology and Plant Pathology, University of California, Riverside, CA, 92521, USA.
[Ti] Título:Rethinking the evolution of eukaryotic metabolism: novel cellular partitioning of enzymes in stramenopiles links serine biosynthesis to glycolysis in mitochondria.
[So] Source:BMC Evol Biol;17(1):241, 2017 Dec 04.
[Is] ISSN:1471-2148
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: An important feature of eukaryotic evolution is metabolic compartmentalization, in which certain pathways are restricted to the cytosol or specific organelles. Glycolysis in eukaryotes is described as a cytosolic process. The universality of this canon has been challenged by recent genome data that suggest that some glycolytic enzymes made by stramenopiles bear mitochondrial targeting peptides. RESULTS: Mining of oomycete, diatom, and brown algal genomes indicates that stramenopiles encode two forms of enzymes for the second half of glycolysis, one with and the other without mitochondrial targeting peptides. The predicted mitochondrial targeting was confirmed by using fluorescent tags to localize phosphoglycerate kinase, phosphoglycerate mutase, and pyruvate kinase in Phytophthora infestans, the oomycete that causes potato blight. A genome-wide search for other enzymes with atypical mitochondrial locations identified phosphoglycerate dehydrogenase, phosphoserine aminotransferase, and phosphoserine phosphatase, which form a pathway for generating serine from the glycolytic intermediate 3-phosphoglycerate. Fluorescent tags confirmed the delivery of these serine biosynthetic enzymes to P. infestans mitochondria. A cytosolic form of this serine biosynthetic pathway, which occurs in most eukaryotes, is missing from oomycetes and most other stramenopiles. The glycolysis and serine metabolism pathways of oomycetes appear to be mosaics of enzymes with different ancestries. While some of the noncanonical oomycete mitochondrial enzymes have the closest affinity in phylogenetic analyses with proteins from other stramenopiles, others cluster with bacterial, plant, or animal proteins. The genes encoding the mitochondrial phosphoglycerate kinase and serine-forming enzymes are physically linked on oomycete chromosomes, which suggests a shared origin. CONCLUSIONS: Stramenopile metabolism appears to have been shaped through the acquisition of genes by descent and lateral or endosymbiotic gene transfer, along with the targeting of the proteins to locations that are novel compared to other eukaryotes. Colocalization of the glycolytic and serine biosynthesis enzymes in mitochondria is apparently necessary since they share a common intermediate. The results indicate that descriptions of metabolism in textbooks do not cover the full diversity of eukaryotic biology.
[Mh] Termos MeSH primário: Evolução Biológica
Células Eucarióticas/metabolismo
Glicólise
Mitocôndrias/metabolismo
Serina/biossíntese
Estramenópilas/enzimologia
Estramenópilas/metabolismo
[Mh] Termos MeSH secundário: Animais
Citosol
Genes
Mitocôndrias/genética
Oomicetos/metabolismo
Fosforilação
Filogenia
Phytophthora infestans/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
452VLY9402 (Serine)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171206
[St] Status:MEDLINE
[do] DOI:10.1186/s12862-017-1087-8


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[PMID]:28463416
[Au] Autor:Kaja S; Payne AJ; Naumchuk Y; Koulen P
[Ad] Endereço:Departments of Ophthalmology and Molecular Pharmacology & Therapeutics, Stritch School of Medicine, Loyola University Chicago, Maywood, Illinois.
[Ti] Título:Quantification of Lactate Dehydrogenase for Cell Viability Testing Using Cell Lines and Primary Cultured Astrocytes.
[So] Source:Curr Protoc Toxicol;72:2.26.1-2.26.10, 2017 May 02.
[Is] ISSN:1934-9262
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Drug discovery heavily relies on cell viability studies to assess the potential toxicity of drug candidates. L-Lactate dehydrogenase (LDH) is a cytoplasmic enzyme that catalyzes the concomitant interconversions of pyruvate to L-lactate and NADH to NAD during glycolysis, and the reverse reactions during the Cori cycle. In response to cellular damage, induced by endogenous cellular mechanisms or as a result of exogenously applied insults, LDH is released from the cytoplasm into the extracellular environment. Its stability in cell culture medium makes it a well-suited correlate for the presence of damage and toxicity in tissues and cells. We herein present protocols for a reproducible and validated LDH assay optimized for several cell types. In contrast to commercially available LDH assays, often associated with proprietary formulations and high cost, our protocols provide ample opportunities for experiment-specific optimization with low variability and cost. © 2017 by John Wiley & Sons, Inc.
[Mh] Termos MeSH primário: Astrócitos/enzimologia
Sobrevivência Celular
L-Lactato Desidrogenase/análise
Toxicologia/métodos
[Mh] Termos MeSH secundário: Animais
Técnicas de Cultura de Células
Linhagem Celular
Linhagem Celular Tumoral
Meios de Cultura/química
Citoplasma/enzimologia
Espaço Extracelular/enzimologia
Glicólise
Seres Humanos
Neurônios/efeitos dos fármacos
Fármacos Neuroprotetores/farmacologia
Nervo Óptico/citologia
Nervo Óptico/efeitos dos fármacos
Cultura Primária de Células
Ratos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Culture Media); 0 (Neuroprotective Agents); EC 1.1.1.27 (L-Lactate Dehydrogenase)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.1002/cptx.21


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[PMID]:28453233
[Au] Autor:Huang YP; Chang NW
[Ad] Endereço:Department of Physiology, College of Medicine, China Medical University, Taichung, Taiwan.
[Ti] Título:Proteomic analysis of oral cancer reveals new potential therapeutic targets involved in the Warburg effect.
[So] Source:Clin Exp Pharmacol Physiol;44(8):880-887, 2017 Aug.
[Is] ISSN:1440-1681
[Cp] País de publicação:Australia
[La] Idioma:eng
[Ab] Resumo:Activation of peroxisome proliferator-activated receptor alpha (PPARα) has been reported to disrupt tumour metabolism and to promote anticancer activity through interfering with the Warburg effect. This study is to investigate whether Warburg effect-related proteins also could be identified in oral tumour lesions and to explore the functional significance of PPARα in metabolic shift. Five pairs of tongue tumour tissues and adjacent reference tissues obtained from 4-NQO/arecoline induced mouse model were analyzed by 2-d-gel-electrophoresis and LC-MS. Further, the hexokinase II level, pyruvate dehydrogenase (PDH) activity, and metabolites of glycolysis and TCA cycle were all examined in order to validate the effect of PPARα on metabolic shift. Changes in protein expression levels revealed that seven proteins, which were involved in glycolysis, the tricarboxylic acid cycle, and the respiratory chain, were down-regulated in tumour tissues. We found that activation of PPARα through fenofibrate could inhibit oral cancer cell growth and switch the way of energy production from the Warburg effect to oxidative phosphorylation. Fenofibrate induced a reduction of hexokinase II protein levels, increases in PDH activity and metabolites of the TCA cycle, and an impairment of ATP production. These findings suggested that activation of the PPARα to reprogram the metabolic pathway might impair the Warburg effect and trigger cancer cell death. The study provides a novel view of changes in protein expression profiles involved in the Warburg effect during oral tumourigenesis. Activation of the PPARα to impair the Warburg effect might offer a new strategy for oral cancer treatment.
[Mh] Termos MeSH primário: Terapia de Alvo Molecular
Neoplasias Bucais/tratamento farmacológico
Neoplasias Bucais/metabolismo
Proteômica
[Mh] Termos MeSH secundário: Animais
Ciclo do Ácido Cítrico/efeitos dos fármacos
Glicólise/efeitos dos fármacos
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Neoplasias Bucais/patologia
Fosforilação Oxidativa/efeitos dos fármacos
PPAR alfa/metabolismo
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (PPAR alpha)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1111/1440-1681.12774


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[PMID]:29302038
[Au] Autor:Lucas S; Omata Y; Hofmann J; Böttcher M; Iljazovic A; Sarter K; Albrecht O; Schulz O; Krishnacoumar B; Krönke G; Herrmann M; Mougiakakos D; Strowig T; Schett G; Zaiss MM
[Ad] Endereço:Department of Internal Medicine 3, Rheumatology and Immunology, Friedrich-Alexander-University Erlangen-Nürnberg (FAU) and Universitätsklinikum Erlangen, 91054, Erlangen, Germany.
[Ti] Título:Short-chain fatty acids regulate systemic bone mass and protect from pathological bone loss.
[So] Source:Nat Commun;9(1):55, 2018 01 04.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Microbial metabolites are known to modulate immune responses of the host. The main metabolites derived from microbial fermentation of dietary fibers in the intestine, short-chain fatty acids (SCFA), affect local and systemic immune functions. Here we show that SCFA are regulators of osteoclast metabolism and bone mass in vivo. Treatment of mice with SCFA as well as feeding with a high-fiber diet significantly increases bone mass and prevents postmenopausal and inflammation-induced bone loss. The protective effects of SCFA on bone mass are associated with inhibition of osteoclast differentiation and bone resorption in vitro and in vivo, while bone formation is not affected. Mechanistically, propionate (C3) and butyrate (C4) induce metabolic reprogramming of osteoclasts resulting in enhanced glycolysis at the expense of oxidative phosphorylation, thereby downregulating essential osteoclast genes such as TRAF6 and NFATc1. In summary, these data identify SCFA as potent regulators of osteoclast metabolism and bone homeostasis.
[Mh] Termos MeSH primário: Reabsorção Óssea/metabolismo
Osso e Ossos/metabolismo
Ácidos Graxos Voláteis/metabolismo
Osteoclastos/metabolismo
[Mh] Termos MeSH secundário: Animais
Densidade Óssea/efeitos dos fármacos
Reabsorção Óssea/prevenção & controle
Osso e Ossos/efeitos dos fármacos
Butiratos/metabolismo
Butiratos/farmacologia
Fibras na Dieta/administração & dosagem
Ácidos Graxos Voláteis/farmacologia
Feminino
Expressão Gênica/efeitos dos fármacos
Glicólise/efeitos dos fármacos
Seres Humanos
Camundongos Endogâmicos C57BL
Osteoclastos/efeitos dos fármacos
Propionatos/metabolismo
Propionatos/farmacologia
Substâncias Protetoras/metabolismo
Substâncias Protetoras/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Butyrates); 0 (Dietary Fiber); 0 (Fatty Acids, Volatile); 0 (Propionates); 0 (Protective Agents)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180106
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02490-4


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[PMID]:29272757
[Au] Autor:Liu Z; Kuang W; Xu X; Li D; Zhu W; Lan Z; Zhang X
[Ad] Endereço:School of Medicine, Yangtze University, Jingzhou 434000, China.
[Ti] Título:Putative identification of components in Zengye Decoction and their effects on glucose consumption and lipogenesis in insulin-induced insulin-resistant HepG2 cells.
[So] Source:J Chromatogr B Analyt Technol Biomed Life Sci;1073:145-153, 2018 Jan 15.
[Is] ISSN:1873-376X
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Zengye Decoction (ZYD) is a well-known traditional medicine in China used for treating diseases associated with "Yin deficiency" such as diabetes. However, little information is available on its components, pharmacological effects and underlying mechanisms. This study was designed to identify its active components and evaluate the effects and mechanisms of ZYD on glucose consumption and lipogenesis in insulin-induced insulin-resistant (IR)-HepG2 cells. In this study, 45 compounds of ZYD were putatively identified, in which the iridoid glycosides such as catalpol, aucubin and harpagide were identified as the main components. The insulin-resistant (IR)-HepG2 cell model was established and the effect of ZYD at three doses (0.17, 0.5 and 1.5 µg/mL) on cell growth was evaluated with an IncuCyte™ live-cell imaging system. The effects of ZYD on glucose consumption and uptake were evaluated by glucose consumption and uptake assay. Meanwhile, the effect of ZYD on lipogenesis was investigated in IR-HepG2 cells by oil red O (ORO) staining. Western blot was applied to observe the changes in some of the key factors involved in glucose metabolism and lipogenesis. It was found that the ZYD at a dose of 1.5 µg/mL exhibited an inhibitory activity on IR-HepG2 cell growth. Besides, ZYD at doses of 0.5 and 1.5 µg/mL accelerated the glucose consumption, glucose uptake and reduced the lipogenesis in the IR-HepG2 cells. Western blot studies revealed that ZYD phosphorylated AMP-activated protein kinase α subunits (AMPKα), upregulated hexokinase (HK), phosphorylated acetyl-CoA carboxylase alpha (pACC1) and carnitine palmitoyltransferase 1A (CPT1A) in the IR-HepG2 cells. These results indicate ZYD promotes glucose consumption and uptake, and attenuates lipogenesis in IR-HepG2 cells, which may be involved in activating AMPK and regulating its downstream factors including HK, pACC1 and CPT1A.
[Mh] Termos MeSH primário: Medicamentos de Ervas Chinesas/farmacologia
Glucose/metabolismo
Resistência à Insulina
Insulina/metabolismo
Lipogênese/efeitos dos fármacos
[Mh] Termos MeSH secundário: Proteínas Quinases Ativadas por AMP/metabolismo
Glicólise/efeitos dos fármacos
Células Hep G2
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Drugs, Chinese Herbal); 0 (Insulin); EC 2.7.11.31 (AMP-Activated Protein Kinases); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180302
[Lr] Data última revisão:
180302
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171223
[St] Status:MEDLINE


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[PMID]:29360449
[Au] Autor:Hua S; Liu C; Liu L; Wu D
[Ad] Endereço:Department of Radiation Oncology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China. Electronic address: huashengni0401@163.com.
[Ti] Título:miR-142-3p inhibits aerobic glycolysis and cell proliferation in hepatocellular carcinoma via targeting LDHA.
[So] Source:Biochem Biophys Res Commun;496(3):947-954, 2018 02 12.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cancer cells are addictively dependent on glycolysis even in an oxygen-rich condition. However, the mechanism underlying micro (mi)RNA regulation of aerobic glycolysis in cancer cells has not been fully understood. Here, we demonstrated that the expression of miR-142-3p was lower in hepatocellular carcinoma (HCC) as compared to adjacent non-tumor samples, which was confirmed in The Cancer Genome Atlas (TCGA) HCC cohorts and Gene Expression Omnibus (GEO) datasets. Function and pathway analysis showed that miR-142-3p was most relevent with metabolism. As predicted, the overexpression of miR-142-3p inhibited aerobic glycolysis and thus proliferation of HCC cells. Mechanistically, we identified lactate dehydrogenase A (LDHA), one of the important catalyticase for aerobic glycolysis, as the target of miR-142-3p. Exogenous expression of miR-142-3p reduced the protein levels of LDHA in both SK-Hep-1 and Huh7 cells. Dual luciferase report assays showed the expression of LDHA was directly modulated by miR-142-3p. miR-142-3p-induced deduction of aerobic glycolysis and proliferation were reversed by LDHA overexpression. Taken together, these results indicate that miR-142-3p could act as a tumor suppressor in HCC by targeting LDHA, suggesting new therapeutic targets for HCC treatment.
[Mh] Termos MeSH primário: Carcinoma Hepatocelular/metabolismo
Proliferação Celular
Regulação Neoplásica da Expressão Gênica/genética
Glucose/metabolismo
Lactato Desidrogenases/metabolismo
Neoplasias Hepáticas/metabolismo
MicroRNAs/metabolismo
[Mh] Termos MeSH secundário: Aerobiose
Carcinoma Hepatocelular/patologia
Glicólise
Seres Humanos
Neoplasias Hepáticas/patologia
Oxigênio/metabolismo
Ligação Proteica
Células Tumorais Cultivadas
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (MIRN142 microRNA, human); 0 (MicroRNAs); EC 1.1.- (Lactate Dehydrogenases); EC 1.1.1.28 (D-lactate dehydrogenase); IY9XDZ35W2 (Glucose); S88TT14065 (Oxygen)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180124
[St] Status:MEDLINE


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[PMID]:29287724
[Au] Autor:Kang H; Jo A; Kim H; Khang R; Lee JY; Kim H; Park CH; Choi JY; Lee Y; Shin JH
[Ad] Endereço:Division of Pharmacology, Department of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Samsung Biomedical Research Institute, Suwon 440-746, South Korea.
[Ti] Título:PARIS reprograms glucose metabolism by HIF-1α induction in dopaminergic neurodegeneration.
[So] Source:Biochem Biophys Res Commun;495(4):2498-2504, 2018 01 22.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Our previous study found that PARIS (ZNF746) transcriptionally suppressed transketolase (TKT), a key enzyme in pentose phosphate pathway (PPP) in the substantia nigra (SN) of AAV-PARIS injected mice. In this study, we revealed that PARIS overexpression reprogrammed glucose metabolic pathway, leading to the increment of glycolytic proteins along with TKT reduction in the SN of AAV-PARIS injected mice. Knock-down of TKT in differentiated SH-SY5Y cells led to an increase of glycolytic enzymes and decrease of PPP-related enzymes whereas overexpression of TKT restored PARIS-mediated glucose metabolic shift, suggesting that glucose metabolic alteration by PARIS is TKT-dependent. Inhibition of PPP by either PARIS overexpression or TKT knock-down elevated the level of H O , and diminished NADPH and GSH levels, ultimately triggering the induction of HIF-1α, a master activator of glycolysis. In addition, TKT inhibition by stereotaxic injection of oxythiamine demonstrated slight decrement of dopaminergic neurons (DNs) in SN but not cortical neurons in the cortex, suggesting that TKT might be a survival factor of DNs. In differentiated SH-SY5Y, cell toxicity by GFP-PARIS was partially restored by introduction of Flag-TKT and siRNA-HIF-1α. We also observed the increase of HIF-1α and glycolytic hexokinase 2 in the SN of Parkinson's disease patients. Taken together, these results suggest that PARIS accumulation might distort the balance of glucose metabolism, providing clues for understanding mechanism underlying selective DNs death by PARIS.
[Mh] Termos MeSH primário: Encéfalo/metabolismo
Neurônios Dopaminérgicos/metabolismo
Glucose/metabolismo
Subunidade alfa do Fator 1 Induzível por Hipóxia/metabolismo
Doença de Parkinson/metabolismo
Proteínas Repressoras/metabolismo
Transcetolase/metabolismo
[Mh] Termos MeSH secundário: Animais
Apoptose
Encéfalo/patologia
Linhagem Celular
Neurônios Dopaminérgicos/patologia
Glicólise
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Doença de Parkinson/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Hif1a protein, mouse); 0 (Hypoxia-Inducible Factor 1, alpha Subunit); 0 (Repressor Proteins); 0 (ZNF746 protein, mouse); EC 2.2.1.1 (Transketolase); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171231
[St] Status:MEDLINE


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[PMID]:29374702
[Au] Autor:Ferreira L; Vitorino R; Neuparth MJ; Rodrigues D; Gama A; Faustino-Rocha AI; Ferreira R; Oliveira PA
[Ad] Endereço:Organic Chemistry, Natural Products and Foodstuffs (QOPNA), Mass Spectrometry Center, University of Aveiro, Aveiro, Portugal.
[Ti] Título:Intense Pulsed Light: Friend or Foe? Molecular Evidence to Clarify Doubts.
[So] Source:Anticancer Res;38(2):779-786, 2018 02.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIM: Intense pulsed light (IPL) has been extensively applied in the field of dermatology and aesthetics; however, the long-term consequences of its use are poorly unknown, and to the best of our knowledge there is no study on the effect of IPL in neoplastic lesions. In order to better understand the molecular mechanisms underlying IPL application in the skin, we used an animal model of carcinogenesis obtained by chemical induction with 12-dimethylbenz(a)anthracene (DMBA) and 12-O-tetradecanoylphorbol-13-acetate (TPA). MATERIALS AND METHODS: Institute of Cancer Research (ICR) mice were administered DMBA and/or TPA and treated with IPL. Skin was evaluated by histopathology and 2DE-blot-MS/MS analysis. RESULTS: Our data evidenced an inflammatory response and a metabolic remodeling of skin towards a glycolytic phenotype after chronic exposure to IPL, which was accomplished by increased oxidative stress and susceptibility to apoptosis. These alterations induced by IPL were more notorious in the DMBA sensitized skin. Keratins and metabolic proteins seem to be the more susceptible to oxidative modifications that might result in loss of function, contributing for the histological changes observed in treated skin. CONCLUSION: Data highlight the deleterious impact of IPL on skin phenotype, which justifies the need for more experimental studies in order to increase our understanding of the IPL long-term safety.
[Mh] Termos MeSH primário: Terapia de Luz Pulsada Intensa/efeitos adversos
Neoplasias Cutâneas/etiologia
Pele/efeitos da radiação
[Mh] Termos MeSH secundário: 9,10-Dimetil-1,2-benzantraceno/administração & dosagem
Animais
Apoptose/efeitos dos fármacos
Apoptose/efeitos da radiação
Carcinógenos/administração & dosagem
Modelos Animais de Doenças
Feminino
Glicólise
Queratinas/metabolismo
Camundongos
Camundongos Endogâmicos ICR
Estresse Oxidativo/efeitos dos fármacos
Estresse Oxidativo/efeitos da radiação
Distribuição Aleatória
Pele/efeitos dos fármacos
Pele/metabolismo
Pele/patologia
Neoplasias Cutâneas/induzido quimicamente
Neoplasias Cutâneas/metabolismo
Neoplasias Cutâneas/patologia
Acetato de Tetradecanoilforbol/administração & dosagem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Carcinogens); 57-97-6 (9,10-Dimethyl-1,2-benzanthracene); 68238-35-7 (Keratins); NI40JAQ945 (Tetradecanoylphorbol Acetate)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180221
[Lr] Data última revisão:
180221
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180129
[St] Status:MEDLINE



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