Glucose utilization via glycogen phosphorylase sustains proliferation and prevents premature senescence in cancer cells
Metabolic reprogramming of cancer cells provides energy and multiple intermediates critical for cell growth. Hypoxia in tumors represents a hostile environment that can encourage these transformations. We report that glycogen metabolism is upregulated in tumors in vivo and in cancer cells in vitro i...
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| Vydané v: | Cell metabolism Ročník 16; číslo 6; s. 751 |
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| Hlavní autori: | , , , , , , , , , , , , |
| Médium: | Journal Article |
| Jazyk: | English |
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United States
05.12.2012
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| ISSN: | 1932-7420, 1932-7420 |
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| Abstract | Metabolic reprogramming of cancer cells provides energy and multiple intermediates critical for cell growth. Hypoxia in tumors represents a hostile environment that can encourage these transformations. We report that glycogen metabolism is upregulated in tumors in vivo and in cancer cells in vitro in response to hypoxia. In vitro, hypoxia induced an early accumulation of glycogen, followed by a gradual decline. Concordantly, glycogen synthase (GYS1) showed a rapid induction, followed by a later increase of glycogen phosphorylase (PYGL). PYGL depletion and the consequent glycogen accumulation led to increased reactive oxygen species (ROS) levels that contributed to a p53-dependent induction of senescence and markedly impaired tumorigenesis in vivo. Metabolic analyses indicated that glycogen degradation by PYGL is important for the optimal function of the pentose phosphate pathway. Thus, glycogen metabolism is a key pathway induced by hypoxia, necessary for optimal glucose utilization, which represents a targetable mechanism of metabolic adaptation. |
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| AbstractList | Metabolic reprogramming of cancer cells provides energy and multiple intermediates critical for cell growth. Hypoxia in tumors represents a hostile environment that can encourage these transformations. We report that glycogen metabolism is upregulated in tumors in vivo and in cancer cells in vitro in response to hypoxia. In vitro, hypoxia induced an early accumulation of glycogen, followed by a gradual decline. Concordantly, glycogen synthase (GYS1) showed a rapid induction, followed by a later increase of glycogen phosphorylase (PYGL). PYGL depletion and the consequent glycogen accumulation led to increased reactive oxygen species (ROS) levels that contributed to a p53-dependent induction of senescence and markedly impaired tumorigenesis in vivo. Metabolic analyses indicated that glycogen degradation by PYGL is important for the optimal function of the pentose phosphate pathway. Thus, glycogen metabolism is a key pathway induced by hypoxia, necessary for optimal glucose utilization, which represents a targetable mechanism of metabolic adaptation. Metabolic reprogramming of cancer cells provides energy and multiple intermediates critical for cell growth. Hypoxia in tumors represents a hostile environment that can encourage these transformations. We report that glycogen metabolism is upregulated in tumors in vivo and in cancer cells in vitro in response to hypoxia. In vitro, hypoxia induced an early accumulation of glycogen, followed by a gradual decline. Concordantly, glycogen synthase (GYS1) showed a rapid induction, followed by a later increase of glycogen phosphorylase (PYGL). PYGL depletion and the consequent glycogen accumulation led to increased reactive oxygen species (ROS) levels that contributed to a p53-dependent induction of senescence and markedly impaired tumorigenesis in vivo. Metabolic analyses indicated that glycogen degradation by PYGL is important for the optimal function of the pentose phosphate pathway. Thus, glycogen metabolism is a key pathway induced by hypoxia, necessary for optimal glucose utilization, which represents a targetable mechanism of metabolic adaptation.Metabolic reprogramming of cancer cells provides energy and multiple intermediates critical for cell growth. Hypoxia in tumors represents a hostile environment that can encourage these transformations. We report that glycogen metabolism is upregulated in tumors in vivo and in cancer cells in vitro in response to hypoxia. In vitro, hypoxia induced an early accumulation of glycogen, followed by a gradual decline. Concordantly, glycogen synthase (GYS1) showed a rapid induction, followed by a later increase of glycogen phosphorylase (PYGL). PYGL depletion and the consequent glycogen accumulation led to increased reactive oxygen species (ROS) levels that contributed to a p53-dependent induction of senescence and markedly impaired tumorigenesis in vivo. Metabolic analyses indicated that glycogen degradation by PYGL is important for the optimal function of the pentose phosphate pathway. Thus, glycogen metabolism is a key pathway induced by hypoxia, necessary for optimal glucose utilization, which represents a targetable mechanism of metabolic adaptation. |
| Author | Li, Ji-Liang Ferguson, David J P Harris, Adrian L Favaro, Elena Bensaad, Karim Tennant, Daniel A Steers, Graham Turley, Helen Chong, Mei G Günther, Ulrich L Snell, Cameron Buffa, Francesca M McIntyre, Alan |
| Author_xml | – sequence: 1 givenname: Elena surname: Favaro fullname: Favaro, Elena organization: Molecular Oncology Laboratories, Weatherall Institute of Molecular Medicine, University of Oxford, John Radcliffe Hospital, Oxford OX3 9DS, UK – sequence: 2 givenname: Karim surname: Bensaad fullname: Bensaad, Karim – sequence: 3 givenname: Mei G surname: Chong fullname: Chong, Mei G – sequence: 4 givenname: Daniel A surname: Tennant fullname: Tennant, Daniel A – sequence: 5 givenname: David J P surname: Ferguson fullname: Ferguson, David J P – sequence: 6 givenname: Cameron surname: Snell fullname: Snell, Cameron – sequence: 7 givenname: Graham surname: Steers fullname: Steers, Graham – sequence: 8 givenname: Helen surname: Turley fullname: Turley, Helen – sequence: 9 givenname: Ji-Liang surname: Li fullname: Li, Ji-Liang – sequence: 10 givenname: Ulrich L surname: Günther fullname: Günther, Ulrich L – sequence: 11 givenname: Francesca M surname: Buffa fullname: Buffa, Francesca M – sequence: 12 givenname: Alan surname: McIntyre fullname: McIntyre, Alan – sequence: 13 givenname: Adrian L surname: Harris fullname: Harris, Adrian L |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/23177934$$D View this record in MEDLINE/PubMed |
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| SubjectTerms | Angiogenesis Inhibitors - pharmacology Animals Antibodies, Monoclonal, Humanized - pharmacology Bevacizumab Breast Neoplasms - metabolism Breast Neoplasms - pathology Cell Hypoxia - drug effects Cell Line, Tumor Cell Proliferation - drug effects Cellular Senescence - drug effects Female Glucose - pharmacology Glycogen - metabolism Glycogen Phosphorylase - antagonists & inhibitors Glycogen Phosphorylase - genetics Glycogen Phosphorylase - metabolism Glycogen Synthase - metabolism HCT116 Cells Humans MCF-7 Cells Mice Mice, Nude Reactive Oxygen Species - metabolism RNA Interference RNA, Small Interfering - metabolism Transplantation, Heterologous Tumor Suppressor Protein p53 - metabolism |
| Title | Glucose utilization via glycogen phosphorylase sustains proliferation and prevents premature senescence in cancer cells |
| URI | https://www.ncbi.nlm.nih.gov/pubmed/23177934 https://www.proquest.com/docview/1237090664 |
| Volume | 16 |
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