Hypoxia induces a lipogenic cancer cell phenotype via HIF1α-dependent and -independent pathways
The biochemistry of cancer cells diverges significantly from normal cells as a result of a comprehensive reprogramming of metabolic pathways. A major factor influencing cancer metabolism is hypoxia, which is mediated by HIF1α and HIF2α. HIF1α represents one of the principal regulators of metabolism...
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| creator | Valli, Alessandro Rodriguez, Miguel Moutsianas, Loukas Fischer, Roman Fedele, Vita Huang, Hong-Lei Van Stiphout, Ruud Jones, Dylan Mccarthy, Michael Vinaxia, Maria Igarashi, Kaori Sato, Maya Soga, Tomoyoshi Buffa, Francesca Mccullagh, James Yanes, Oscar Harris, Adrian Kessler, Benedikt |
| description | The biochemistry of cancer cells diverges significantly from normal cells as a result of a comprehensive reprogramming of metabolic pathways. A major factor influencing cancer metabolism is hypoxia, which is mediated by HIF1α and HIF2α. HIF1α represents one of the principal regulators of metabolism and energetic balance in cancer cells through its regulation of glycolysis, glycogen synthesis, Krebs cycle and the pentose phosphate shunt. However, less is known about the role of HIF1α in modulating lipid metabolism. Lipids serve cancer cells to provide molecules acting as oncogenic signals, energetic reserve, precursors for new membrane synthesis and to balance redox biological reactions. To study the role of HIF1α in these processes, we used HCT116 colorectal cancer cells expressing endogenous HIF1α and cells in which the hif1α gene was deleted to characterize HIF1α-dependent and independent effects on hypoxia regulated lipid metabolites. Untargeted metabolomics integrated with proteomics revealed that hypoxia induced many changes in lipids metabolites. Enzymatic steps in fatty acid synthesis and the Kennedy pathway were modified in a HIF1α-dependent fashion. Palmitate, stearate, PLD3 and PAFC16 were regulated in a HIF-independent manner. Our results demonstrate the impact of hypoxia on lipid metabolites, of which a distinct subset is regulated by HIF1α. |
| doi_str_mv | 10.18632/oncotarget.3058 |
| format | Article |
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A major factor influencing cancer metabolism is hypoxia, which is mediated by HIF1α and HIF2α. HIF1α represents one of the principal regulators of metabolism and energetic balance in cancer cells through its regulation of glycolysis, glycogen synthesis, Krebs cycle and the pentose phosphate shunt. However, less is known about the role of HIF1α in modulating lipid metabolism. Lipids serve cancer cells to provide molecules acting as oncogenic signals, energetic reserve, precursors for new membrane synthesis and to balance redox biological reactions. To study the role of HIF1α in these processes, we used HCT116 colorectal cancer cells expressing endogenous HIF1α and cells in which the hif1α gene was deleted to characterize HIF1α-dependent and independent effects on hypoxia regulated lipid metabolites. Untargeted metabolomics integrated with proteomics revealed that hypoxia induced many changes in lipids metabolites. Enzymatic steps in fatty acid synthesis and the Kennedy pathway were modified in a HIF1α-dependent fashion. Palmitate, stearate, PLD3 and PAFC16 were regulated in a HIF-independent manner. Our results demonstrate the impact of hypoxia on lipid metabolites, of which a distinct subset is regulated by HIF1α.</description><identifier>ISSN: 1949-2553</identifier><identifier>EISSN: 1949-2553</identifier><identifier>DOI: 10.18632/oncotarget.3058</identifier><identifier>PMID: 25605240</identifier><language>eng</language><publisher>United States: Impact Journals LLC</publisher><subject>Acetyl-CoA C-Acyltransferase - genetics ; Acetyl-CoA C-Acyltransferase - metabolism ; Acetyl-CoA Carboxylase - genetics ; Acetyl-CoA Carboxylase - metabolism ; Aged ; Basic Helix-Loop-Helix Transcription Factors - genetics ; Basic Helix-Loop-Helix Transcription Factors - metabolism ; Blotting, Western ; Cell Hypoxia ; Cell Line, Tumor ; Colorectal Neoplasms - genetics ; Colorectal Neoplasms - metabolism ; Colorectal Neoplasms - pathology ; Fatty Acids - biosynthesis ; Female ; Genomics - methods ; HCT116 Cells ; Humans ; Hypoxia-Inducible Factor 1, alpha Subunit - genetics ; Hypoxia-Inducible Factor 1, alpha Subunit - metabolism ; Lipid Metabolism ; Lipids - biosynthesis ; Male ; Metabolomics - methods ; Middle Aged ; Platelet Activating Factor - genetics ; Platelet Activating Factor - metabolism ; Priority Research Paper ; Proteomics - methods ; RNA Interference ; Signal Transduction</subject><ispartof>Oncotarget, 2015-02, Vol.6 (4), p.1920-1941</ispartof><rights>Copyright: © 2015 Valli et al. 2015</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c396t-dd81380ed53b62d3e644e9ddd5a361a3f21ccd52ebc741773827a843e9963cbe3</citedby><cites>FETCH-LOGICAL-c396t-dd81380ed53b62d3e644e9ddd5a361a3f21ccd52ebc741773827a843e9963cbe3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4385826/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4385826/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25605240$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Valli, Alessandro</creatorcontrib><creatorcontrib>Rodriguez, Miguel</creatorcontrib><creatorcontrib>Moutsianas, Loukas</creatorcontrib><creatorcontrib>Fischer, Roman</creatorcontrib><creatorcontrib>Fedele, Vita</creatorcontrib><creatorcontrib>Huang, Hong-Lei</creatorcontrib><creatorcontrib>Van Stiphout, Ruud</creatorcontrib><creatorcontrib>Jones, Dylan</creatorcontrib><creatorcontrib>Mccarthy, Michael</creatorcontrib><creatorcontrib>Vinaxia, Maria</creatorcontrib><creatorcontrib>Igarashi, Kaori</creatorcontrib><creatorcontrib>Sato, Maya</creatorcontrib><creatorcontrib>Soga, Tomoyoshi</creatorcontrib><creatorcontrib>Buffa, Francesca</creatorcontrib><creatorcontrib>Mccullagh, James</creatorcontrib><creatorcontrib>Yanes, Oscar</creatorcontrib><creatorcontrib>Harris, Adrian</creatorcontrib><creatorcontrib>Kessler, Benedikt</creatorcontrib><title>Hypoxia induces a lipogenic cancer cell phenotype via HIF1α-dependent and -independent pathways</title><title>Oncotarget</title><addtitle>Oncotarget</addtitle><description>The biochemistry of cancer cells diverges significantly from normal cells as a result of a comprehensive reprogramming of metabolic pathways. A major factor influencing cancer metabolism is hypoxia, which is mediated by HIF1α and HIF2α. HIF1α represents one of the principal regulators of metabolism and energetic balance in cancer cells through its regulation of glycolysis, glycogen synthesis, Krebs cycle and the pentose phosphate shunt. However, less is known about the role of HIF1α in modulating lipid metabolism. Lipids serve cancer cells to provide molecules acting as oncogenic signals, energetic reserve, precursors for new membrane synthesis and to balance redox biological reactions. To study the role of HIF1α in these processes, we used HCT116 colorectal cancer cells expressing endogenous HIF1α and cells in which the hif1α gene was deleted to characterize HIF1α-dependent and independent effects on hypoxia regulated lipid metabolites. Untargeted metabolomics integrated with proteomics revealed that hypoxia induced many changes in lipids metabolites. Enzymatic steps in fatty acid synthesis and the Kennedy pathway were modified in a HIF1α-dependent fashion. Palmitate, stearate, PLD3 and PAFC16 were regulated in a HIF-independent manner. 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A major factor influencing cancer metabolism is hypoxia, which is mediated by HIF1α and HIF2α. HIF1α represents one of the principal regulators of metabolism and energetic balance in cancer cells through its regulation of glycolysis, glycogen synthesis, Krebs cycle and the pentose phosphate shunt. However, less is known about the role of HIF1α in modulating lipid metabolism. Lipids serve cancer cells to provide molecules acting as oncogenic signals, energetic reserve, precursors for new membrane synthesis and to balance redox biological reactions. To study the role of HIF1α in these processes, we used HCT116 colorectal cancer cells expressing endogenous HIF1α and cells in which the hif1α gene was deleted to characterize HIF1α-dependent and independent effects on hypoxia regulated lipid metabolites. Untargeted metabolomics integrated with proteomics revealed that hypoxia induced many changes in lipids metabolites. Enzymatic steps in fatty acid synthesis and the Kennedy pathway were modified in a HIF1α-dependent fashion. Palmitate, stearate, PLD3 and PAFC16 were regulated in a HIF-independent manner. Our results demonstrate the impact of hypoxia on lipid metabolites, of which a distinct subset is regulated by HIF1α.</abstract><cop>United States</cop><pub>Impact Journals LLC</pub><pmid>25605240</pmid><doi>10.18632/oncotarget.3058</doi><tpages>22</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Oncotarget, 2015-02, Vol.6 (4), p.1920-1941 |
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| subjects | Acetyl-CoA C-Acyltransferase - genetics Acetyl-CoA C-Acyltransferase - metabolism Acetyl-CoA Carboxylase - genetics Acetyl-CoA Carboxylase - metabolism Aged Basic Helix-Loop-Helix Transcription Factors - genetics Basic Helix-Loop-Helix Transcription Factors - metabolism Blotting, Western Cell Hypoxia Cell Line, Tumor Colorectal Neoplasms - genetics Colorectal Neoplasms - metabolism Colorectal Neoplasms - pathology Fatty Acids - biosynthesis Female Genomics - methods HCT116 Cells Humans Hypoxia-Inducible Factor 1, alpha Subunit - genetics Hypoxia-Inducible Factor 1, alpha Subunit - metabolism Lipid Metabolism Lipids - biosynthesis Male Metabolomics - methods Middle Aged Platelet Activating Factor - genetics Platelet Activating Factor - metabolism Priority Research Paper Proteomics - methods RNA Interference Signal Transduction |
| title | Hypoxia induces a lipogenic cancer cell phenotype via HIF1α-dependent and -independent pathways |
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