IL-1β maintains the redox balance by regulating glutaredoxin 1 expression during oral carcinogenesis.
Identifieur interne : 000355 ( Main/Exploration ); précédent : 000354; suivant : 000356IL-1β maintains the redox balance by regulating glutaredoxin 1 expression during oral carcinogenesis.
Auteurs : Xijuan Chen [République populaire de Chine] ; Qianshu Lv [République populaire de Chine] ; Yun Hong [République populaire de Chine] ; Xiaobing Chen [République populaire de Chine] ; Bin Cheng [République populaire de Chine] ; Tong Wu [République populaire de Chine]Source :
- Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology [ 1600-0714 ] ; 2017.
Descripteurs français
- KwdFr :
- Animaux (MeSH), Carcinome épidermoïde (métabolisme), Espèces réactives de l'oxygène (métabolisme), Glutarédoxines (métabolisme), Humains (MeSH), Interleukine-1 bêta (métabolisme), Mâle (MeSH), Oxydoréduction (MeSH), Rat Sprague-Dawley (MeSH), Rats (MeSH), Régulation de l'expression des gènes tumoraux (MeSH), Transformation cellulaire néoplasique (métabolisme), Tumeurs de la bouche (métabolisme).
- MESH :
English descriptors
- KwdEn :
- Animals (MeSH), Carcinoma, Squamous Cell (metabolism), Cell Transformation, Neoplastic (metabolism), Gene Expression Regulation, Neoplastic (MeSH), Glutaredoxins (metabolism), Humans (MeSH), Interleukin-1beta (metabolism), Male (MeSH), Mouth Neoplasms (metabolism), Oxidation-Reduction (MeSH), Rats (MeSH), Rats, Sprague-Dawley (MeSH), Reactive Oxygen Species (metabolism).
- MESH :
- chemical , metabolism : Glutaredoxins, Interleukin-1beta, Reactive Oxygen Species.
- metabolism : Carcinoma, Squamous Cell, Cell Transformation, Neoplastic, Mouth Neoplasms.
- Animals, Gene Expression Regulation, Neoplastic, Humans, Male, Oxidation-Reduction, Rats, Rats, Sprague-Dawley.
Abstract
BACKGROUND
Interleukin-1 beta (IL-1β) is a pleiotropic cancer-inflammation-linked cytokine which has been reported upregulated in many cancers. In our previous study, IL-1β was found to be one of the key node genes during oral malignant transformation, and glutaredoxin 1 (Grx1) was identified as one of the downstream genes of IL-1β in tumor microenvironment. Grx1 is ubiquitous oxidoreductase which is necessary for scavenging reactive oxygen species (ROS) and the intracellular redox balance maintenance.
METHODS
Tissues from different stages of mucosal malignant transformation were obtained from 4NQO-induced rat oral carcinogenesis model and human mucosa for Grx1 expression detection by immunohistochemical staining. The intracellular ROS levels and Grx1 mRNA level of oral squamous carcinoma cell CAL27 were detected after IL-1β treatment with or without pretreatment of IL-1Ra or NAC, respectively. The ROS levels were detected in Leti-si-IL-1β and Leti-si-NC CAL27 cells after IL-1β stimulation. The invasion and migration abilities of CAL27 cells were tested by transwell assay after IL-1β stimulation with or without pretreatment of IL-1Ra.
RESULTS
Grx1 expression was associated with the malignant transformation process in vivo. Exogenous IL-1β upregulated the intracellular ROS level and the expression of Grx1 in CAL27 cells, which could be counteracted by IL-1Ra. The intracellular ROS accumulation induced by exogenous IL-1β was responsible for the Grx1 upregulation. Endogenous IL-1β acted as a switch in regulating the ROS level by modulating Grx1 expression, which was involved in the invasion and migration of OSCC cells.
CONCLUSIONS
IL-1β finely orchestrated the redox balance during carcinogenesis by modulating Grx1 expression.
DOI: 10.1111/jop.12502
PubMed: 27658048
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term>
<term>Carcinoma, Squamous Cell (metabolism)</term>
<term>Cell Transformation, Neoplastic (metabolism)</term>
<term>Gene Expression Regulation, Neoplastic (MeSH)</term>
<term>Glutaredoxins (metabolism)</term>
<term>Humans (MeSH)</term>
<term>Interleukin-1beta (metabolism)</term>
<term>Male (MeSH)</term>
<term>Mouth Neoplasms (metabolism)</term>
<term>Oxidation-Reduction (MeSH)</term>
<term>Rats (MeSH)</term>
<term>Rats, Sprague-Dawley (MeSH)</term>
<term>Reactive Oxygen Species (metabolism)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Animaux (MeSH)</term>
<term>Carcinome épidermoïde (métabolisme)</term>
<term>Espèces réactives de l'oxygène (métabolisme)</term>
<term>Glutarédoxines (métabolisme)</term>
<term>Humains (MeSH)</term>
<term>Interleukine-1 bêta (métabolisme)</term>
<term>Mâle (MeSH)</term>
<term>Oxydoréduction (MeSH)</term>
<term>Rat Sprague-Dawley (MeSH)</term>
<term>Rats (MeSH)</term>
<term>Régulation de l'expression des gènes tumoraux (MeSH)</term>
<term>Transformation cellulaire néoplasique (métabolisme)</term>
<term>Tumeurs de la bouche (métabolisme)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Glutaredoxins</term>
<term>Interleukin-1beta</term>
<term>Reactive Oxygen Species</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Carcinoma, Squamous Cell</term>
<term>Cell Transformation, Neoplastic</term>
<term>Mouth Neoplasms</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Carcinome épidermoïde</term>
<term>Espèces réactives de l'oxygène</term>
<term>Glutarédoxines</term>
<term>Interleukine-1 bêta</term>
<term>Transformation cellulaire néoplasique</term>
<term>Tumeurs de la bouche</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Gene Expression Regulation, Neoplastic</term>
<term>Humans</term>
<term>Male</term>
<term>Oxidation-Reduction</term>
<term>Rats</term>
<term>Rats, Sprague-Dawley</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Animaux</term>
<term>Humains</term>
<term>Mâle</term>
<term>Oxydoréduction</term>
<term>Rat Sprague-Dawley</term>
<term>Rats</term>
<term>Régulation de l'expression des gènes tumoraux</term>
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<front><div type="abstract" xml:lang="en"><p><b>BACKGROUND</b>
</p>
<p>Interleukin-1 beta (IL-1β) is a pleiotropic cancer-inflammation-linked cytokine which has been reported upregulated in many cancers. In our previous study, IL-1β was found to be one of the key node genes during oral malignant transformation, and glutaredoxin 1 (Grx1) was identified as one of the downstream genes of IL-1β in tumor microenvironment. Grx1 is ubiquitous oxidoreductase which is necessary for scavenging reactive oxygen species (ROS) and the intracellular redox balance maintenance.</p>
</div>
<div type="abstract" xml:lang="en"><p><b>METHODS</b>
</p>
<p>Tissues from different stages of mucosal malignant transformation were obtained from 4NQO-induced rat oral carcinogenesis model and human mucosa for Grx1 expression detection by immunohistochemical staining. The intracellular ROS levels and Grx1 mRNA level of oral squamous carcinoma cell CAL27 were detected after IL-1β treatment with or without pretreatment of IL-1Ra or NAC, respectively. The ROS levels were detected in Leti-si-IL-1β and Leti-si-NC CAL27 cells after IL-1β stimulation. The invasion and migration abilities of CAL27 cells were tested by transwell assay after IL-1β stimulation with or without pretreatment of IL-1Ra.</p>
</div>
<div type="abstract" xml:lang="en"><p><b>RESULTS</b>
</p>
<p>Grx1 expression was associated with the malignant transformation process in vivo. Exogenous IL-1β upregulated the intracellular ROS level and the expression of Grx1 in CAL27 cells, which could be counteracted by IL-1Ra. The intracellular ROS accumulation induced by exogenous IL-1β was responsible for the Grx1 upregulation. Endogenous IL-1β acted as a switch in regulating the ROS level by modulating Grx1 expression, which was involved in the invasion and migration of OSCC cells.</p>
</div>
<div type="abstract" xml:lang="en"><p><b>CONCLUSIONS</b>
</p>
<p>IL-1β finely orchestrated the redox balance during carcinogenesis by modulating Grx1 expression.</p>
</div>
</front>
</TEI>
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<DateCompleted><Year>2018</Year>
<Month>04</Month>
<Day>04</Day>
</DateCompleted>
<DateRevised><Year>2018</Year>
<Month>04</Month>
<Day>04</Day>
</DateRevised>
<Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1600-0714</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>46</Volume>
<Issue>5</Issue>
<PubDate><Year>2017</Year>
<Month>May</Month>
</PubDate>
</JournalIssue>
<Title>Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology</Title>
<ISOAbbreviation>J Oral Pathol Med</ISOAbbreviation>
</Journal>
<ArticleTitle>IL-1β maintains the redox balance by regulating glutaredoxin 1 expression during oral carcinogenesis.</ArticleTitle>
<Pagination><MedlinePgn>332-339</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1111/jop.12502</ELocationID>
<Abstract><AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">Interleukin-1 beta (IL-1β) is a pleiotropic cancer-inflammation-linked cytokine which has been reported upregulated in many cancers. In our previous study, IL-1β was found to be one of the key node genes during oral malignant transformation, and glutaredoxin 1 (Grx1) was identified as one of the downstream genes of IL-1β in tumor microenvironment. Grx1 is ubiquitous oxidoreductase which is necessary for scavenging reactive oxygen species (ROS) and the intracellular redox balance maintenance.</AbstractText>
<AbstractText Label="METHODS" NlmCategory="METHODS">Tissues from different stages of mucosal malignant transformation were obtained from 4NQO-induced rat oral carcinogenesis model and human mucosa for Grx1 expression detection by immunohistochemical staining. The intracellular ROS levels and Grx1 mRNA level of oral squamous carcinoma cell CAL27 were detected after IL-1β treatment with or without pretreatment of IL-1Ra or NAC, respectively. The ROS levels were detected in Leti-si-IL-1β and Leti-si-NC CAL27 cells after IL-1β stimulation. The invasion and migration abilities of CAL27 cells were tested by transwell assay after IL-1β stimulation with or without pretreatment of IL-1Ra.</AbstractText>
<AbstractText Label="RESULTS" NlmCategory="RESULTS">Grx1 expression was associated with the malignant transformation process in vivo. Exogenous IL-1β upregulated the intracellular ROS level and the expression of Grx1 in CAL27 cells, which could be counteracted by IL-1Ra. The intracellular ROS accumulation induced by exogenous IL-1β was responsible for the Grx1 upregulation. Endogenous IL-1β acted as a switch in regulating the ROS level by modulating Grx1 expression, which was involved in the invasion and migration of OSCC cells.</AbstractText>
<AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">IL-1β finely orchestrated the redox balance during carcinogenesis by modulating Grx1 expression.</AbstractText>
<CopyrightInformation>© 2016 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Chen</LastName>
<ForeName>Xijuan</ForeName>
<Initials>X</Initials>
<AffiliationInfo><Affiliation>Department of Oral Medicine, Hospital of Stomatology, Guangzhou, Guangdong, China.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Guangdong Provincial Key Laboratory of Stomatology, Guanghua School of Stomatology, Sun Yat-sen University, Guangzhou, Guangdong, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Lv</LastName>
<ForeName>Qianshu</ForeName>
<Initials>Q</Initials>
<AffiliationInfo><Affiliation>Department of Oral Medicine, Affiliated Zhongshan Hospital, Sun Yat-sen University, Zhongshan, Guangdong, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Hong</LastName>
<ForeName>Yun</ForeName>
<Initials>Y</Initials>
<AffiliationInfo><Affiliation>Department of Oral Medicine, Hospital of Stomatology, Guangzhou, Guangdong, China.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Guangdong Provincial Key Laboratory of Stomatology, Guanghua School of Stomatology, Sun Yat-sen University, Guangzhou, Guangdong, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Chen</LastName>
<ForeName>Xiaobing</ForeName>
<Initials>X</Initials>
<AffiliationInfo><Affiliation>Department of Oral Medicine, Hospital of Stomatology, Guangzhou, Guangdong, China.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Guangdong Provincial Key Laboratory of Stomatology, Guanghua School of Stomatology, Sun Yat-sen University, Guangzhou, Guangdong, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Cheng</LastName>
<ForeName>Bin</ForeName>
<Initials>B</Initials>
<AffiliationInfo><Affiliation>Department of Oral Medicine, Hospital of Stomatology, Guangzhou, Guangdong, China.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Guangdong Provincial Key Laboratory of Stomatology, Guanghua School of Stomatology, Sun Yat-sen University, Guangzhou, Guangdong, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Wu</LastName>
<ForeName>Tong</ForeName>
<Initials>T</Initials>
<AffiliationInfo><Affiliation>Department of Oral Medicine, Hospital of Stomatology, Guangzhou, Guangdong, China.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Guangdong Provincial Key Laboratory of Stomatology, Guanghua School of Stomatology, Sun Yat-sen University, Guangzhou, Guangdong, China.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType>
</PublicationTypeList>
<ArticleDate DateType="Electronic"><Year>2016</Year>
<Month>10</Month>
<Day>14</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>Denmark</Country>
<MedlineTA>J Oral Pathol Med</MedlineTA>
<NlmUniqueID>8911934</NlmUniqueID>
<ISSNLinking>0904-2512</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D054477">Glutaredoxins</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D053583">Interleukin-1beta</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D017382">Reactive Oxygen Species</NameOfSubstance>
</Chemical>
</ChemicalList>
<CitationSubset>D</CitationSubset>
<CitationSubset>IM</CitationSubset>
<MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D002294" MajorTopicYN="N">Carcinoma, Squamous Cell</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D002471" MajorTopicYN="N">Cell Transformation, Neoplastic</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D015972" MajorTopicYN="N">Gene Expression Regulation, Neoplastic</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D054477" MajorTopicYN="N">Glutaredoxins</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D053583" MajorTopicYN="N">Interleukin-1beta</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D009062" MajorTopicYN="N">Mouth Neoplasms</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D010084" MajorTopicYN="Y">Oxidation-Reduction</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D051381" MajorTopicYN="N">Rats</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D017207" MajorTopicYN="N">Rats, Sprague-Dawley</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D017382" MajorTopicYN="N">Reactive Oxygen Species</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
</MeshHeadingList>
<KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Grx1</Keyword>
<Keyword MajorTopicYN="N">IL-1β</Keyword>
<Keyword MajorTopicYN="N">oral squamous cell carcinoma</Keyword>
<Keyword MajorTopicYN="N">reactive oxygen species</Keyword>
<Keyword MajorTopicYN="N">redox balance</Keyword>
</KeywordList>
</MedlineCitation>
<PubmedData><History><PubMedPubDate PubStatus="accepted"><Year>2016</Year>
<Month>09</Month>
<Day>15</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="pubmed"><Year>2016</Year>
<Month>9</Month>
<Day>23</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="medline"><Year>2018</Year>
<Month>4</Month>
<Day>5</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="entrez"><Year>2016</Year>
<Month>9</Month>
<Day>23</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
</History>
<PublicationStatus>ppublish</PublicationStatus>
<ArticleIdList><ArticleId IdType="pubmed">27658048</ArticleId>
<ArticleId IdType="doi">10.1111/jop.12502</ArticleId>
</ArticleIdList>
</PubmedData>
</pubmed>
<affiliations><list><country><li>République populaire de Chine</li>
</country>
</list>
<tree><country name="République populaire de Chine"><noRegion><name sortKey="Chen, Xijuan" sort="Chen, Xijuan" uniqKey="Chen X" first="Xijuan" last="Chen">Xijuan Chen</name>
</noRegion>
<name sortKey="Chen, Xiaobing" sort="Chen, Xiaobing" uniqKey="Chen X" first="Xiaobing" last="Chen">Xiaobing Chen</name>
<name sortKey="Chen, Xiaobing" sort="Chen, Xiaobing" uniqKey="Chen X" first="Xiaobing" last="Chen">Xiaobing Chen</name>
<name sortKey="Chen, Xijuan" sort="Chen, Xijuan" uniqKey="Chen X" first="Xijuan" last="Chen">Xijuan Chen</name>
<name sortKey="Cheng, Bin" sort="Cheng, Bin" uniqKey="Cheng B" first="Bin" last="Cheng">Bin Cheng</name>
<name sortKey="Cheng, Bin" sort="Cheng, Bin" uniqKey="Cheng B" first="Bin" last="Cheng">Bin Cheng</name>
<name sortKey="Hong, Yun" sort="Hong, Yun" uniqKey="Hong Y" first="Yun" last="Hong">Yun Hong</name>
<name sortKey="Hong, Yun" sort="Hong, Yun" uniqKey="Hong Y" first="Yun" last="Hong">Yun Hong</name>
<name sortKey="Lv, Qianshu" sort="Lv, Qianshu" uniqKey="Lv Q" first="Qianshu" last="Lv">Qianshu Lv</name>
<name sortKey="Wu, Tong" sort="Wu, Tong" uniqKey="Wu T" first="Tong" last="Wu">Tong Wu</name>
<name sortKey="Wu, Tong" sort="Wu, Tong" uniqKey="Wu T" first="Tong" last="Wu">Tong Wu</name>
</country>
</tree>
</affiliations>
</record>
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