Protein S-glutathionylation induced by hypoxia increases hypoxia-inducible factor-1α in human colon cancer cells.
Identifieur interne : 000233 ( Main/Exploration ); précédent : 000232; suivant : 000234Protein S-glutathionylation induced by hypoxia increases hypoxia-inducible factor-1α in human colon cancer cells.
Auteurs : Daun Jeon [Corée du Sud] ; Heon Joo Park [Corée du Sud] ; Hong Seok Kim [Corée du Sud]Source :
- Biochemical and biophysical research communications [ 1090-2104 ] ; 2018.
Descripteurs français
- KwdFr :
- Glutathion (métabolisme), Humains (MeSH), Hypoxie (complications), Hypoxie (génétique), Hypoxie (métabolisme), Hypoxie cellulaire (MeSH), Oxydoréduction (MeSH), Régulation de l'expression des gènes tumoraux (MeSH), Sous-unité alpha du facteur-1 induit par l'hypoxie (métabolisme), Tumeurs du côlon (complications), Tumeurs du côlon (génétique), Tumeurs du côlon (métabolisme).
- MESH :
English descriptors
- KwdEn :
- Cell Hypoxia (MeSH), Colonic Neoplasms (complications), Colonic Neoplasms (genetics), Colonic Neoplasms (metabolism), Gene Expression Regulation, Neoplastic (MeSH), Glutathione (metabolism), Humans (MeSH), Hypoxia (complications), Hypoxia (genetics), Hypoxia (metabolism), Hypoxia-Inducible Factor 1, alpha Subunit (metabolism), Oxidation-Reduction (MeSH).
- MESH :
- chemical , metabolism : Glutathione, Hypoxia-Inducible Factor 1, alpha Subunit.
- complications : Colonic Neoplasms, Hypoxia.
- genetics : Colonic Neoplasms, Hypoxia.
- metabolism : Colonic Neoplasms, Hypoxia.
- Cell Hypoxia, Gene Expression Regulation, Neoplastic, Humans, Oxidation-Reduction.
Abstract
Hypoxia is a common characteristic of many types of solid tumors. Intratumoral hypoxia selects for tumor cells that survive in a low oxygen environment, undergo epithelial-mesenchymal transition, are more motile and invasive, and show gene expression changes driven by hypoxia-inducible factor-1α (HIF-1α) activation. Therefore, targeting HIF-1α is an attractive strategy for disrupting multiple pathways crucial for tumor growth. In the present study, we demonstrated that hypoxia increases the S-glutathionylation of HIF-1α and its protein levels in colon cancer cells. This effect is significantly prevented by decreasing oxidized glutathione as well as glutathione depletion, indicating that S-glutathionylation and the formation of protein-glutathione mixed disulfides is related to HIF-1α protein levels. Moreover, colon cancer cells expressing glutaredoxin 1 are resistant to inducing HIF-1α and expressing hypoxia-responsive genes under hypoxic conditions. Therefore, S-glutathionylation of HIF-1α induced by tumor hypoxia may be a novel therapeutic target for the development of new drugs.
DOI: 10.1016/j.bbrc.2017.11.018
PubMed: 29113799
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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Electronic address: kimhs0622@inha.ac.kr.</nlm:affiliation><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Department of Molecular Medicine, Inha University College of Medicine, Incheon 22212, Republic of Korea; Hypoxia-related Disease Research Center, Inha University College of Medicine, Incheon 22212</wicri:regionArea><wicri:noRegion>Incheon 22212</wicri:noRegion></affiliation></author></analytic><series><title level="j">Biochemical and biophysical research communications</title><idno type="eISSN">1090-2104</idno><imprint><date when="2018" type="published">2018</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Cell Hypoxia (MeSH)</term><term>Colonic Neoplasms (complications)</term><term>Colonic Neoplasms (genetics)</term><term>Colonic Neoplasms (metabolism)</term><term>Gene Expression Regulation, Neoplastic (MeSH)</term><term>Glutathione (metabolism)</term><term>Humans (MeSH)</term><term>Hypoxia (complications)</term><term>Hypoxia (genetics)</term><term>Hypoxia (metabolism)</term><term>Hypoxia-Inducible Factor 1, alpha Subunit (metabolism)</term><term>Oxidation-Reduction (MeSH)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Glutathion (métabolisme)</term><term>Humains (MeSH)</term><term>Hypoxie (complications)</term><term>Hypoxie (génétique)</term><term>Hypoxie (métabolisme)</term><term>Hypoxie cellulaire (MeSH)</term><term>Oxydoréduction (MeSH)</term><term>Régulation de l'expression des gènes tumoraux (MeSH)</term><term>Sous-unité alpha du facteur-1 induit par l'hypoxie (métabolisme)</term><term>Tumeurs du côlon (complications)</term><term>Tumeurs du côlon (génétique)</term><term>Tumeurs du côlon (métabolisme)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Glutathione</term><term>Hypoxia-Inducible Factor 1, alpha Subunit</term></keywords><keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Colonic Neoplasms</term><term>Hypoxia</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Colonic Neoplasms</term><term>Hypoxia</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Hypoxie</term><term>Tumeurs du côlon</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Colonic Neoplasms</term><term>Hypoxia</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Glutathion</term><term>Hypoxie</term><term>Sous-unité alpha du facteur-1 induit par l'hypoxie</term><term>Tumeurs du côlon</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Cell Hypoxia</term><term>Gene Expression Regulation, Neoplastic</term><term>Humans</term><term>Oxidation-Reduction</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Humains</term><term>Hypoxie cellulaire</term><term>Oxydoréduction</term><term>Régulation de l'expression des gènes tumoraux</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Hypoxia is a common characteristic of many types of solid tumors. Intratumoral hypoxia selects for tumor cells that survive in a low oxygen environment, undergo epithelial-mesenchymal transition, are more motile and invasive, and show gene expression changes driven by hypoxia-inducible factor-1α (HIF-1α) activation. Therefore, targeting HIF-1α is an attractive strategy for disrupting multiple pathways crucial for tumor growth. In the present study, we demonstrated that hypoxia increases the S-glutathionylation of HIF-1α and its protein levels in colon cancer cells. This effect is significantly prevented by decreasing oxidized glutathione as well as glutathione depletion, indicating that S-glutathionylation and the formation of protein-glutathione mixed disulfides is related to HIF-1α protein levels. Moreover, colon cancer cells expressing glutaredoxin 1 are resistant to inducing HIF-1α and expressing hypoxia-responsive genes under hypoxic conditions. Therefore, S-glutathionylation of HIF-1α induced by tumor hypoxia may be a novel therapeutic target for the development of new drugs.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">29113799</PMID><DateCompleted><Year>2018</Year><Month>01</Month><Day>05</Day></DateCompleted><DateRevised><Year>2018</Year><Month>01</Month><Day>05</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1090-2104</ISSN><JournalIssue CitedMedium="Internet"><Volume>495</Volume><Issue>1</Issue><PubDate><Year>2018</Year><Month>01</Month><Day>01</Day></PubDate></JournalIssue><Title>Biochemical and biophysical research communications</Title><ISOAbbreviation>Biochem Biophys Res Commun</ISOAbbreviation></Journal><ArticleTitle>Protein S-glutathionylation induced by hypoxia increases hypoxia-inducible factor-1α in human colon cancer cells.</ArticleTitle><Pagination><MedlinePgn>212-216</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">S0006-291X(17)32196-4</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.bbrc.2017.11.018</ELocationID><Abstract><AbstractText>Hypoxia is a common characteristic of many types of solid tumors. Intratumoral hypoxia selects for tumor cells that survive in a low oxygen environment, undergo epithelial-mesenchymal transition, are more motile and invasive, and show gene expression changes driven by hypoxia-inducible factor-1α (HIF-1α) activation. Therefore, targeting HIF-1α is an attractive strategy for disrupting multiple pathways crucial for tumor growth. In the present study, we demonstrated that hypoxia increases the S-glutathionylation of HIF-1α and its protein levels in colon cancer cells. This effect is significantly prevented by decreasing oxidized glutathione as well as glutathione depletion, indicating that S-glutathionylation and the formation of protein-glutathione mixed disulfides is related to HIF-1α protein levels. Moreover, colon cancer cells expressing glutaredoxin 1 are resistant to inducing HIF-1α and expressing hypoxia-responsive genes under hypoxic conditions. Therefore, S-glutathionylation of HIF-1α induced by tumor hypoxia may be a novel therapeutic target for the development of new drugs.</AbstractText><CopyrightInformation>Copyright © 2017 Elsevier Inc. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Jeon</LastName><ForeName>Daun</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Department of Molecular Medicine, Inha University College of Medicine, Incheon 22212, Republic of Korea; Hypoxia-related Disease Research Center, Inha University College of Medicine, Incheon 22212, Republic of Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Park</LastName><ForeName>Heon Joo</ForeName><Initials>HJ</Initials><AffiliationInfo><Affiliation>Hypoxia-related Disease Research Center, Inha University College of Medicine, Incheon 22212, Republic of Korea; Department of Microbiology, Inha University College of Medicine, Incheon 22212, Republic of Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kim</LastName><ForeName>Hong Seok</ForeName><Initials>HS</Initials><AffiliationInfo><Affiliation>Department of Molecular Medicine, Inha University College of Medicine, Incheon 22212, Republic of Korea; Hypoxia-related Disease Research Center, Inha University College of Medicine, Incheon 22212, Republic of Korea. Electronic address: kimhs0622@inha.ac.kr.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2017</Year><Month>11</Month><Day>04</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Biochem Biophys Res Commun</MedlineTA><NlmUniqueID>0372516</NlmUniqueID><ISSNLinking>0006-291X</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D051795">Hypoxia-Inducible Factor 1, alpha Subunit</NameOfSubstance></Chemical><Chemical><RegistryNumber>GAN16C9B8O</RegistryNumber><NameOfSubstance UI="D005978">Glutathione</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D015687" MajorTopicYN="N">Cell Hypoxia</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003110" MajorTopicYN="N">Colonic Neoplasms</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015972" MajorTopicYN="N">Gene Expression Regulation, Neoplastic</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005978" MajorTopicYN="N">Glutathione</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000860" MajorTopicYN="N">Hypoxia</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051795" MajorTopicYN="N">Hypoxia-Inducible Factor 1, alpha Subunit</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010084" MajorTopicYN="N">Oxidation-Reduction</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">Colon cancer</Keyword><Keyword MajorTopicYN="Y">Hypoxia</Keyword><Keyword MajorTopicYN="Y">Hypoxia-inducible factor-1α</Keyword><Keyword MajorTopicYN="Y">S-glutathionylation</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2017</Year><Month>10</Month><Day>30</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2017</Year><Month>11</Month><Day>02</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2017</Year><Month>11</Month><Day>9</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2018</Year><Month>1</Month><Day>6</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2017</Year><Month>11</Month><Day>9</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">29113799</ArticleId><ArticleId IdType="pii">S0006-291X(17)32196-4</ArticleId><ArticleId IdType="doi">10.1016/j.bbrc.2017.11.018</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Corée du Sud</li></country></list><tree><country name="Corée du Sud"><noRegion><name sortKey="Jeon, Daun" sort="Jeon, Daun" uniqKey="Jeon D" first="Daun" last="Jeon">Daun Jeon</name></noRegion><name sortKey="Kim, Hong Seok" sort="Kim, Hong Seok" uniqKey="Kim H" first="Hong Seok" last="Kim">Hong Seok Kim</name><name sortKey="Park, Heon Joo" sort="Park, Heon Joo" uniqKey="Park H" first="Heon Joo" last="Park">Heon Joo Park</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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