The role of hypoxia-inducible factors in tumorigenesis
Hypoxia-inducible factors (HIFs) are essential mediators of the cellular oxygen-signaling pathway. They are heterodimeric transcription factors consisting of an oxygen-sensitive alpha subunit (HIF- α ) and a constitutive beta subunit (HIF- β ) that facilitate both oxygen delivery and adaptation to o...
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| Veröffentlicht in: | Cell death and differentiation 2008-04, Vol.15 (4), p.678-685 |
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| description | Hypoxia-inducible factors (HIFs) are essential mediators of the cellular oxygen-signaling pathway. They are heterodimeric transcription factors consisting of an oxygen-sensitive alpha subunit (HIF-
α
) and a constitutive beta subunit (HIF-
β
) that facilitate both oxygen delivery and adaptation to oxygen deprivation by regulating the expression of genes that control glucose uptake, metabolism, angiogenesis, erythropoiesis, cell proliferation, and apoptosis. In most experimental models, the HIF pathway is a positive regulator of tumor growth as its inhibition often results in tumor suppression. In clinical samples, HIF is found elevated and correlates with poor patient prognosis in a variety of cancers. In summary, HIF regulates multiple aspects of tumorigenesis, including angiogenesis, proliferation, metabolism, metastasis, differentiation, and response to radiation therapy, making it a critical regulator of the malignant phenotype. |
| doi_str_mv | 10.1038/cdd.2008.21 |
| format | Article |
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α
) and a constitutive beta subunit (HIF-
β
) that facilitate both oxygen delivery and adaptation to oxygen deprivation by regulating the expression of genes that control glucose uptake, metabolism, angiogenesis, erythropoiesis, cell proliferation, and apoptosis. In most experimental models, the HIF pathway is a positive regulator of tumor growth as its inhibition often results in tumor suppression. In clinical samples, HIF is found elevated and correlates with poor patient prognosis in a variety of cancers. In summary, HIF regulates multiple aspects of tumorigenesis, including angiogenesis, proliferation, metabolism, metastasis, differentiation, and response to radiation therapy, making it a critical regulator of the malignant phenotype.</description><identifier>ISSN: 1350-9047</identifier><identifier>EISSN: 1476-5403</identifier><identifier>DOI: 10.1038/cdd.2008.21</identifier><identifier>PMID: 18259193</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>Adaptation, Physiological ; Angiogenesis ; Animals ; Apoptosis ; Basic Helix-Loop-Helix Transcription Factors - metabolism ; Biochemistry ; Biomedical and Life Sciences ; Cancer ; Cell Biology ; Cell Cycle Analysis ; Cell death ; Cell Differentiation ; Cell growth ; Cell Hypoxia ; Cell Proliferation ; Energy Metabolism ; Gene expression ; Humans ; Hydrocarbons ; Hypoxia ; Hypoxia - genetics ; Hypoxia - metabolism ; Hypoxia - pathology ; Hypoxia-Inducible Factor 1, alpha Subunit - metabolism ; Kinases ; Life Sciences ; Metabolism ; Neoplasm Invasiveness ; Neoplasm Metastasis ; Neoplasms - genetics ; Neoplasms - metabolism ; Neoplasms - pathology ; Neoplasms - radiotherapy ; Neovascularization, Pathologic - metabolism ; Oncology ; Oxygen - metabolism ; Proteins ; Radiation ; review ; Signal Transduction ; Stem Cells ; Transcription factors ; Tumorigenesis</subject><ispartof>Cell death and differentiation, 2008-04, Vol.15 (4), p.678-685</ispartof><rights>Springer Nature Limited 2008</rights><rights>Copyright Nature Publishing Group Apr 2008</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c575t-31ebd55b2f0f5dd7d0a7d6859edba6f18da12cf1ed0e8a5fec3f403d20f4feb3</citedby><cites>FETCH-LOGICAL-c575t-31ebd55b2f0f5dd7d0a7d6859edba6f18da12cf1ed0e8a5fec3f403d20f4feb3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18259193$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Rankin, E B</creatorcontrib><creatorcontrib>Giaccia, A J</creatorcontrib><title>The role of hypoxia-inducible factors in tumorigenesis</title><title>Cell death and differentiation</title><addtitle>Cell Death Differ</addtitle><addtitle>Cell Death Differ</addtitle><description>Hypoxia-inducible factors (HIFs) are essential mediators of the cellular oxygen-signaling pathway. They are heterodimeric transcription factors consisting of an oxygen-sensitive alpha subunit (HIF-
α
) and a constitutive beta subunit (HIF-
β
) that facilitate both oxygen delivery and adaptation to oxygen deprivation by regulating the expression of genes that control glucose uptake, metabolism, angiogenesis, erythropoiesis, cell proliferation, and apoptosis. In most experimental models, the HIF pathway is a positive regulator of tumor growth as its inhibition often results in tumor suppression. In clinical samples, HIF is found elevated and correlates with poor patient prognosis in a variety of cancers. In summary, HIF regulates multiple aspects of tumorigenesis, including angiogenesis, proliferation, metabolism, metastasis, differentiation, and response to radiation therapy, making it a critical regulator of the malignant phenotype.</description><subject>Adaptation, Physiological</subject><subject>Angiogenesis</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Basic Helix-Loop-Helix Transcription Factors - metabolism</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Cancer</subject><subject>Cell Biology</subject><subject>Cell Cycle Analysis</subject><subject>Cell death</subject><subject>Cell Differentiation</subject><subject>Cell growth</subject><subject>Cell Hypoxia</subject><subject>Cell Proliferation</subject><subject>Energy Metabolism</subject><subject>Gene expression</subject><subject>Humans</subject><subject>Hydrocarbons</subject><subject>Hypoxia</subject><subject>Hypoxia - genetics</subject><subject>Hypoxia - metabolism</subject><subject>Hypoxia - pathology</subject><subject>Hypoxia-Inducible Factor 1, alpha Subunit - metabolism</subject><subject>Kinases</subject><subject>Life Sciences</subject><subject>Metabolism</subject><subject>Neoplasm Invasiveness</subject><subject>Neoplasm Metastasis</subject><subject>Neoplasms - genetics</subject><subject>Neoplasms - metabolism</subject><subject>Neoplasms - pathology</subject><subject>Neoplasms - radiotherapy</subject><subject>Neovascularization, Pathologic - metabolism</subject><subject>Oncology</subject><subject>Oxygen - metabolism</subject><subject>Proteins</subject><subject>Radiation</subject><subject>review</subject><subject>Signal Transduction</subject><subject>Stem Cells</subject><subject>Transcription factors</subject><subject>Tumorigenesis</subject><issn>1350-9047</issn><issn>1476-5403</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNptkc1v3CAQxVHVqEk2PfWeWj3k0ng7YGPsS6VqlS8pUi57RxiGXSIvbMGOmv--rHaVNFVOjJjfPB7zCPlCYU6han9oY-YMoJ0z-oGc0Fo0Ja-h-pjrikPZQS2OyWlKjwDQiK75RI5py3hHu-qENMs1FjEMWARbrJ-34Y9TpfNm0q7Pl1bpMcRUOF-M0yZEt0KPyaUzcmTVkPDz4ZyR5fXVcnFb3j_c3C1-3ZeaCz6WFcXecN4zC5YbIwwoYZqWd2h61VjaGkWZthQNYKu4RV3ZbN0wsLXFvpqRn3vZ7dRv0Gj0Y1SD3Ea3UfFZBuXk2453a7kKT7ICDk3ezoxcHARi-D1hGuXGJY3DoDyGKUkBNYBgPIPf_gMfwxR9_ptkVAgmOrqDvu8hHUNKEe2LEwpyl4XMWchdFnko0-f_mn9lD8vPwOUeSLnlVxhf33xf7-se92qcIr7oZWaHZOIvLGufvw</recordid><startdate>20080401</startdate><enddate>20080401</enddate><creator>Rankin, E B</creator><creator>Giaccia, A J</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QP</scope><scope>7QR</scope><scope>7T5</scope><scope>7TK</scope><scope>7TM</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20080401</creationdate><title>The role of hypoxia-inducible factors in tumorigenesis</title><author>Rankin, E B ; Giaccia, A J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c575t-31ebd55b2f0f5dd7d0a7d6859edba6f18da12cf1ed0e8a5fec3f403d20f4feb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Adaptation, Physiological</topic><topic>Angiogenesis</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Basic Helix-Loop-Helix Transcription Factors - metabolism</topic><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Cancer</topic><topic>Cell Biology</topic><topic>Cell Cycle Analysis</topic><topic>Cell death</topic><topic>Cell Differentiation</topic><topic>Cell growth</topic><topic>Cell Hypoxia</topic><topic>Cell Proliferation</topic><topic>Energy Metabolism</topic><topic>Gene expression</topic><topic>Humans</topic><topic>Hydrocarbons</topic><topic>Hypoxia</topic><topic>Hypoxia - genetics</topic><topic>Hypoxia - metabolism</topic><topic>Hypoxia - pathology</topic><topic>Hypoxia-Inducible Factor 1, alpha Subunit - metabolism</topic><topic>Kinases</topic><topic>Life Sciences</topic><topic>Metabolism</topic><topic>Neoplasm Invasiveness</topic><topic>Neoplasm Metastasis</topic><topic>Neoplasms - genetics</topic><topic>Neoplasms - metabolism</topic><topic>Neoplasms - pathology</topic><topic>Neoplasms - radiotherapy</topic><topic>Neovascularization, Pathologic - metabolism</topic><topic>Oncology</topic><topic>Oxygen - metabolism</topic><topic>Proteins</topic><topic>Radiation</topic><topic>review</topic><topic>Signal Transduction</topic><topic>Stem Cells</topic><topic>Transcription factors</topic><topic>Tumorigenesis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Rankin, E B</creatorcontrib><creatorcontrib>Giaccia, A J</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cell death and differentiation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Rankin, E B</au><au>Giaccia, A J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The role of hypoxia-inducible factors in tumorigenesis</atitle><jtitle>Cell death and differentiation</jtitle><stitle>Cell Death Differ</stitle><addtitle>Cell Death Differ</addtitle><date>2008-04-01</date><risdate>2008</risdate><volume>15</volume><issue>4</issue><spage>678</spage><epage>685</epage><pages>678-685</pages><issn>1350-9047</issn><eissn>1476-5403</eissn><abstract>Hypoxia-inducible factors (HIFs) are essential mediators of the cellular oxygen-signaling pathway. They are heterodimeric transcription factors consisting of an oxygen-sensitive alpha subunit (HIF-
α
) and a constitutive beta subunit (HIF-
β
) that facilitate both oxygen delivery and adaptation to oxygen deprivation by regulating the expression of genes that control glucose uptake, metabolism, angiogenesis, erythropoiesis, cell proliferation, and apoptosis. In most experimental models, the HIF pathway is a positive regulator of tumor growth as its inhibition often results in tumor suppression. In clinical samples, HIF is found elevated and correlates with poor patient prognosis in a variety of cancers. In summary, HIF regulates multiple aspects of tumorigenesis, including angiogenesis, proliferation, metabolism, metastasis, differentiation, and response to radiation therapy, making it a critical regulator of the malignant phenotype.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>18259193</pmid><doi>10.1038/cdd.2008.21</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Cell death and differentiation, 2008-04, Vol.15 (4), p.678-685 |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
| subjects | Adaptation, Physiological Angiogenesis Animals Apoptosis Basic Helix-Loop-Helix Transcription Factors - metabolism Biochemistry Biomedical and Life Sciences Cancer Cell Biology Cell Cycle Analysis Cell death Cell Differentiation Cell growth Cell Hypoxia Cell Proliferation Energy Metabolism Gene expression Humans Hydrocarbons Hypoxia Hypoxia - genetics Hypoxia - metabolism Hypoxia - pathology Hypoxia-Inducible Factor 1, alpha Subunit - metabolism Kinases Life Sciences Metabolism Neoplasm Invasiveness Neoplasm Metastasis Neoplasms - genetics Neoplasms - metabolism Neoplasms - pathology Neoplasms - radiotherapy Neovascularization, Pathologic - metabolism Oncology Oxygen - metabolism Proteins Radiation review Signal Transduction Stem Cells Transcription factors Tumorigenesis |
| title | The role of hypoxia-inducible factors in tumorigenesis |
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