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Extracellular Matrix Remodeling Regulates Glucose Metabolism through TXNIP Destabilization.
Sullivan, William J; Mullen, Peter J; Schmid, Ernst W; Flores, Aimee; Momcilovic, Milica; Sharpley, Mark S; Jelinek, David; Whiteley, Andrew E; Maxwell, Matthew B; Wilde, Blake R; Banerjee, Utpal; Coller, Hilary A; Shackelford, David B; Braas, Daniel; Ayer, Donald E; de Aguiar Vallim, Thomas Q; Lowry, William E; Christofk, Heather R.
Afiliación
  • Sullivan WJ; Department of Biological Chemistry, David Geffen School of Medicine, University of California, Los Angeles (UCLA), Los Angeles, CA 90095, USA; Department of Molecular and Medical Pharmacology, David Geffen School of Medicine, UCLA, Los Angeles, CA 90095, USA.
  • Mullen PJ; Department of Biological Chemistry, David Geffen School of Medicine, University of California, Los Angeles (UCLA), Los Angeles, CA 90095, USA.
  • Schmid EW; Department of Biological Chemistry, David Geffen School of Medicine, University of California, Los Angeles (UCLA), Los Angeles, CA 90095, USA.
  • Flores A; Department of Molecular, Cell, and Developmental Biology, UCLA, Los Angeles, CA 90095, USA; Molecular Biology Institute, UCLA, Los Angeles, CA 90095, USA.
  • Momcilovic M; Department of Pulmonary and Critical Care Medicine, David Geffen School of Medicine, UCLA, Los Angeles, CA 90095, USA.
  • Sharpley MS; Department of Molecular, Cell, and Developmental Biology, UCLA, Los Angeles, CA 90095, USA.
  • Jelinek D; Department of Molecular, Cell, and Developmental Biology, UCLA, Los Angeles, CA 90095, USA.
  • Whiteley AE; Department of Biological Chemistry, David Geffen School of Medicine, University of California, Los Angeles (UCLA), Los Angeles, CA 90095, USA.
  • Maxwell MB; Department of Biological Chemistry, David Geffen School of Medicine, University of California, Los Angeles (UCLA), Los Angeles, CA 90095, USA.
  • Wilde BR; Department of Oncological Sciences, Huntsman Cancer Institute, University of Utah, Salt Lake City, UT 84112, USA.
  • Banerjee U; Department of Biological Chemistry, David Geffen School of Medicine, University of California, Los Angeles (UCLA), Los Angeles, CA 90095, USA; Department of Molecular, Cell, and Developmental Biology, UCLA, Los Angeles, CA 90095, USA; Molecular Biology Institute, UCLA, Los Angeles, CA 90095, USA; El
  • Coller HA; Department of Biological Chemistry, David Geffen School of Medicine, University of California, Los Angeles (UCLA), Los Angeles, CA 90095, USA; Department of Molecular, Cell, and Developmental Biology, UCLA, Los Angeles, CA 90095, USA; Eli and Edythe Broad Center of Regenerative Medicine and Stem Cel
  • Shackelford DB; Department of Pulmonary and Critical Care Medicine, David Geffen School of Medicine, UCLA, Los Angeles, CA 90095, USA; Jonsson Comprehensive Cancer Center, UCLA, Los Angeles, CA 90095, USA.
  • Braas D; Department of Molecular and Medical Pharmacology, David Geffen School of Medicine, UCLA, Los Angeles, CA 90095, USA; UCLA Metabolomics Center, Los Angeles, CA 90095, USA.
  • Ayer DE; Department of Oncological Sciences, Huntsman Cancer Institute, University of Utah, Salt Lake City, UT 84112, USA.
  • de Aguiar Vallim TQ; Department of Biological Chemistry, David Geffen School of Medicine, University of California, Los Angeles (UCLA), Los Angeles, CA 90095, USA; Department of Medicine, David Geffen School of Medicine, UCLA, Los Angeles, CA 90095, USA.
  • Lowry WE; Department of Molecular, Cell, and Developmental Biology, UCLA, Los Angeles, CA 90095, USA; Molecular Biology Institute, UCLA, Los Angeles, CA 90095, USA; Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research, UCLA, Los Angeles, CA 90095, USA; Jonsson Comprehensive Cancer Cente
  • Christofk HR; Department of Biological Chemistry, David Geffen School of Medicine, University of California, Los Angeles (UCLA), Los Angeles, CA 90095, USA; Department of Molecular and Medical Pharmacology, David Geffen School of Medicine, UCLA, Los Angeles, CA 90095, USA; Eli and Edythe Broad Center of Regenerat
Cell ; 175(1): 117-132.e21, 2018 09 20.
Article en En | MEDLINE | ID: mdl-30197082
ABSTRACT
The metabolic state of a cell is influenced by cell-extrinsic factors, including nutrient availability and growth factor signaling. Here, we present extracellular matrix (ECM) remodeling as another fundamental node of cell-extrinsic metabolic regulation. Unbiased analysis of glycolytic drivers identified the hyaluronan-mediated motility receptor as being among the most highly correlated with glycolysis in cancer. Confirming a mechanistic link between the ECM component hyaluronan and metabolism, treatment of cells and xenografts with hyaluronidase triggers a robust increase in glycolysis. This is largely achieved through rapid receptor tyrosine kinase-mediated induction of the mRNA decay factor ZFP36, which targets TXNIP transcripts for degradation. Because TXNIP promotes internalization of the glucose transporter GLUT1, its acute decline enriches GLUT1 at the plasma membrane. Functionally, induction of glycolysis by hyaluronidase is required for concomitant acceleration of cell migration. This interconnection between ECM remodeling and metabolism is exhibited in dynamic tissue states, including tumorigenesis and embryogenesis.
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Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Asunto principal: Proteínas Portadoras / Matriz Extracelular Tipo de estudio: Prognostic_studies Límite: Humans Idioma: En Revista: Cell Año: 2018 Tipo del documento: Article País de afiliación: Estados Unidos
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Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Asunto principal: Proteínas Portadoras / Matriz Extracelular Tipo de estudio: Prognostic_studies Límite: Humans Idioma: En Revista: Cell Año: 2018 Tipo del documento: Article País de afiliación: Estados Unidos