Hypoxia promotes ligand-independent EGF receptor signaling via hypoxia-inducible factor–mediated upregulation of caveolin-1
Caveolin-1 (CAV1) is an essential structural constituent of caveolae, specialized lipid raft microdomains on the cell membrane involved in endocytosis and signal transduction, which are inexplicably deregulated and are associated with aggressiveness in numerous cancers. Here we identify CAV1 as a di...
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| Veröffentlicht in: | Proceedings of the National Academy of Sciences - PNAS 2012-03, Vol.109 (13), p.4892-4897 |
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| creator | Wang, Yi Roche, Olga Xu, Chaoying Moriyama, Eduardo H Heir, Pardeep Chung, Jacky Roos, Frederik C Chen, Yonghong Finak, Greg Milosevic, Michael Wilson, Brian C Teh, Bin Tean Park, Morag Irwin, Meredith S Ohh, Michael |
| description | Caveolin-1 (CAV1) is an essential structural constituent of caveolae, specialized lipid raft microdomains on the cell membrane involved in endocytosis and signal transduction, which are inexplicably deregulated and are associated with aggressiveness in numerous cancers. Here we identify CAV1 as a direct transcriptional target of oxygen-labile hypoxia-inducible factor 1 and 2 that accentuates the formation of caveolae, leading to increased dimerization of EGF receptor within the confined surface area of caveolae and its subsequent phosphorylation in the absence of ligand. Hypoxia-inducible factor–dependent up-regulation of CAV1 enhanced the oncogenic potential of tumor cells by increasing the cell proliferative, migratory, and invasive capacities. These results support a concept in which a crisis in oxygen availability or a tumor exhibiting hypoxic signature triggers caveolae formation that bypasses the requirement for ligand engagement to initiate receptor activation and the critical downstream adaptive signaling during a period when ligands required to activate these receptors are limited or are not yet available. |
| doi_str_mv | 10.1073/pnas.1112129109 |
| format | Article |
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Here we identify CAV1 as a direct transcriptional target of oxygen-labile hypoxia-inducible factor 1 and 2 that accentuates the formation of caveolae, leading to increased dimerization of EGF receptor within the confined surface area of caveolae and its subsequent phosphorylation in the absence of ligand. Hypoxia-inducible factor–dependent up-regulation of CAV1 enhanced the oncogenic potential of tumor cells by increasing the cell proliferative, migratory, and invasive capacities. These results support a concept in which a crisis in oxygen availability or a tumor exhibiting hypoxic signature triggers caveolae formation that bypasses the requirement for ligand engagement to initiate receptor activation and the critical downstream adaptive signaling during a period when ligands required to activate these receptors are limited or are not yet available.</description><identifier>ISSN: 0027-8424</identifier><identifier>EISSN: 1091-6490</identifier><identifier>DOI: 10.1073/pnas.1112129109</identifier><identifier>PMID: 22411794</identifier><language>eng</language><publisher>United States: National Academy of Sciences</publisher><subject>Base Sequence ; Basic Helix-Loop-Helix Transcription Factors ; Basic Helix-Loop-Helix Transcription Factors - metabolism ; Biological Sciences ; Cancer ; Caveolae ; Caveolae - metabolism ; Caveolae - ultrastructure ; Caveolin 1 ; Caveolin 1 - metabolism ; Cell growth ; Cell Hypoxia ; Cell Line, Tumor ; cell membranes ; Cell Proliferation ; Conserved Sequence ; Conserved Sequence - genetics ; dimerization ; ErbB Receptors ; Gene expression regulation ; genetics ; HeLa cells ; Humans ; Hypoxia ; Hypoxia-Inducible Factor 1 ; Hypoxia-Inducible Factor 1 - metabolism ; Ligands ; MAP Kinase Signaling System ; metabolism ; Molecular Sequence Data ; neoplasms ; Oxygen ; Phosphorylation ; Protein Binding ; Receptor, Epidermal Growth Factor - metabolism ; Receptors ; Renal cell carcinoma ; Response Elements ; Response Elements - genetics ; RNA Polymerase II ; RNA Polymerase II - metabolism ; Signal Transduction ; surface area ; Transcription, Genetic ; Tumors ; ultrastructure ; Up-Regulation ; Von Hippel-Lindau Tumor Suppressor Protein ; Von Hippel-Lindau Tumor Suppressor Protein - metabolism</subject><ispartof>Proceedings of the National Academy of Sciences - PNAS, 2012-03, Vol.109 (13), p.4892-4897</ispartof><rights>copyright © 1993-2008 National Academy of Sciences of the United States of America</rights><rights>Copyright National Academy of Sciences Mar 27, 2012</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c588t-3b82021f8dbde999ad587774b55c5671d9e2679800e98a2e04c3cedec9fe97893</citedby><cites>FETCH-LOGICAL-c588t-3b82021f8dbde999ad587774b55c5671d9e2679800e98a2e04c3cedec9fe97893</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Uhttp://www.pnas.org/content/109/13.cover.gif</thumbnail><linktopdf>$$Uhttps://www.jstor.org/stable/pdf/41588392$$EPDF$$P50$$Gjstor$$H</linktopdf><linktohtml>$$Uhttps://www.jstor.org/stable/41588392$$EHTML$$P50$$Gjstor$$H</linktohtml><link.rule.ids>230,314,723,776,780,799,881,27901,27902,53766,53768,57992,58225</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22411794$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Yi</creatorcontrib><creatorcontrib>Roche, Olga</creatorcontrib><creatorcontrib>Xu, Chaoying</creatorcontrib><creatorcontrib>Moriyama, Eduardo H</creatorcontrib><creatorcontrib>Heir, Pardeep</creatorcontrib><creatorcontrib>Chung, Jacky</creatorcontrib><creatorcontrib>Roos, Frederik C</creatorcontrib><creatorcontrib>Chen, Yonghong</creatorcontrib><creatorcontrib>Finak, Greg</creatorcontrib><creatorcontrib>Milosevic, Michael</creatorcontrib><creatorcontrib>Wilson, Brian C</creatorcontrib><creatorcontrib>Teh, Bin Tean</creatorcontrib><creatorcontrib>Park, Morag</creatorcontrib><creatorcontrib>Irwin, Meredith S</creatorcontrib><creatorcontrib>Ohh, Michael</creatorcontrib><title>Hypoxia promotes ligand-independent EGF receptor signaling via hypoxia-inducible factor–mediated upregulation of caveolin-1</title><title>Proceedings of the National Academy of Sciences - PNAS</title><addtitle>Proc Natl Acad Sci U S A</addtitle><description>Caveolin-1 (CAV1) is an essential structural constituent of caveolae, specialized lipid raft microdomains on the cell membrane involved in endocytosis and signal transduction, which are inexplicably deregulated and are associated with aggressiveness in numerous cancers. Here we identify CAV1 as a direct transcriptional target of oxygen-labile hypoxia-inducible factor 1 and 2 that accentuates the formation of caveolae, leading to increased dimerization of EGF receptor within the confined surface area of caveolae and its subsequent phosphorylation in the absence of ligand. Hypoxia-inducible factor–dependent up-regulation of CAV1 enhanced the oncogenic potential of tumor cells by increasing the cell proliferative, migratory, and invasive capacities. These results support a concept in which a crisis in oxygen availability or a tumor exhibiting hypoxic signature triggers caveolae formation that bypasses the requirement for ligand engagement to initiate receptor activation and the critical downstream adaptive signaling during a period when ligands required to activate these receptors are limited or are not yet available.</description><subject>Base Sequence</subject><subject>Basic Helix-Loop-Helix Transcription Factors</subject><subject>Basic Helix-Loop-Helix Transcription Factors - metabolism</subject><subject>Biological Sciences</subject><subject>Cancer</subject><subject>Caveolae</subject><subject>Caveolae - metabolism</subject><subject>Caveolae - ultrastructure</subject><subject>Caveolin 1</subject><subject>Caveolin 1 - metabolism</subject><subject>Cell growth</subject><subject>Cell Hypoxia</subject><subject>Cell Line, Tumor</subject><subject>cell membranes</subject><subject>Cell Proliferation</subject><subject>Conserved Sequence</subject><subject>Conserved Sequence - genetics</subject><subject>dimerization</subject><subject>ErbB Receptors</subject><subject>Gene expression regulation</subject><subject>genetics</subject><subject>HeLa cells</subject><subject>Humans</subject><subject>Hypoxia</subject><subject>Hypoxia-Inducible Factor 1</subject><subject>Hypoxia-Inducible Factor 1 - metabolism</subject><subject>Ligands</subject><subject>MAP Kinase Signaling System</subject><subject>metabolism</subject><subject>Molecular Sequence Data</subject><subject>neoplasms</subject><subject>Oxygen</subject><subject>Phosphorylation</subject><subject>Protein Binding</subject><subject>Receptor, Epidermal Growth Factor - metabolism</subject><subject>Receptors</subject><subject>Renal cell carcinoma</subject><subject>Response Elements</subject><subject>Response Elements - genetics</subject><subject>RNA Polymerase II</subject><subject>RNA Polymerase II - metabolism</subject><subject>Signal Transduction</subject><subject>surface area</subject><subject>Transcription, Genetic</subject><subject>Tumors</subject><subject>ultrastructure</subject><subject>Up-Regulation</subject><subject>Von Hippel-Lindau Tumor Suppressor Protein</subject><subject>Von Hippel-Lindau Tumor Suppressor Protein - 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metabolism</topic><topic>Receptors</topic><topic>Renal cell carcinoma</topic><topic>Response Elements</topic><topic>Response Elements - genetics</topic><topic>RNA Polymerase II</topic><topic>RNA Polymerase II - metabolism</topic><topic>Signal Transduction</topic><topic>surface area</topic><topic>Transcription, Genetic</topic><topic>Tumors</topic><topic>ultrastructure</topic><topic>Up-Regulation</topic><topic>Von Hippel-Lindau Tumor Suppressor Protein</topic><topic>Von Hippel-Lindau Tumor Suppressor Protein - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wang, Yi</creatorcontrib><creatorcontrib>Roche, Olga</creatorcontrib><creatorcontrib>Xu, Chaoying</creatorcontrib><creatorcontrib>Moriyama, Eduardo H</creatorcontrib><creatorcontrib>Heir, Pardeep</creatorcontrib><creatorcontrib>Chung, Jacky</creatorcontrib><creatorcontrib>Roos, Frederik C</creatorcontrib><creatorcontrib>Chen, Yonghong</creatorcontrib><creatorcontrib>Finak, Greg</creatorcontrib><creatorcontrib>Milosevic, Michael</creatorcontrib><creatorcontrib>Wilson, Brian C</creatorcontrib><creatorcontrib>Teh, Bin Tean</creatorcontrib><creatorcontrib>Park, Morag</creatorcontrib><creatorcontrib>Irwin, Meredith S</creatorcontrib><creatorcontrib>Ohh, Michael</creatorcontrib><collection>AGRIS</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>AGRICOLA</collection><collection>AGRICOLA - 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Here we identify CAV1 as a direct transcriptional target of oxygen-labile hypoxia-inducible factor 1 and 2 that accentuates the formation of caveolae, leading to increased dimerization of EGF receptor within the confined surface area of caveolae and its subsequent phosphorylation in the absence of ligand. Hypoxia-inducible factor–dependent up-regulation of CAV1 enhanced the oncogenic potential of tumor cells by increasing the cell proliferative, migratory, and invasive capacities. These results support a concept in which a crisis in oxygen availability or a tumor exhibiting hypoxic signature triggers caveolae formation that bypasses the requirement for ligand engagement to initiate receptor activation and the critical downstream adaptive signaling during a period when ligands required to activate these receptors are limited or are not yet available.</abstract><cop>United States</cop><pub>National Academy of Sciences</pub><pmid>22411794</pmid><doi>10.1073/pnas.1112129109</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Proceedings of the National Academy of Sciences - PNAS, 2012-03, Vol.109 (13), p.4892-4897 |
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| subjects | Base Sequence Basic Helix-Loop-Helix Transcription Factors Basic Helix-Loop-Helix Transcription Factors - metabolism Biological Sciences Cancer Caveolae Caveolae - metabolism Caveolae - ultrastructure Caveolin 1 Caveolin 1 - metabolism Cell growth Cell Hypoxia Cell Line, Tumor cell membranes Cell Proliferation Conserved Sequence Conserved Sequence - genetics dimerization ErbB Receptors Gene expression regulation genetics HeLa cells Humans Hypoxia Hypoxia-Inducible Factor 1 Hypoxia-Inducible Factor 1 - metabolism Ligands MAP Kinase Signaling System metabolism Molecular Sequence Data neoplasms Oxygen Phosphorylation Protein Binding Receptor, Epidermal Growth Factor - metabolism Receptors Renal cell carcinoma Response Elements Response Elements - genetics RNA Polymerase II RNA Polymerase II - metabolism Signal Transduction surface area Transcription, Genetic Tumors ultrastructure Up-Regulation Von Hippel-Lindau Tumor Suppressor Protein Von Hippel-Lindau Tumor Suppressor Protein - metabolism |
| title | Hypoxia promotes ligand-independent EGF receptor signaling via hypoxia-inducible factor–mediated upregulation of caveolin-1 |
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