Receptor for Advanced Glycation End Products Acts as a Fuel to Colorectal Cancer Development.
Identifieur interne : 000060 ( Main/Exploration ); précédent : 000059; suivant : 000061Receptor for Advanced Glycation End Products Acts as a Fuel to Colorectal Cancer Development.
Auteurs : Fatemeh Azizian-Farsani [Iran] ; Navid Abedpoor [Iran] ; Mohammad Hasan Sheikhha [Iran] ; Ali Osmay Gure [Turquie] ; Mohammad Hossein Nasr-Esfahani [Iran] ; Kamran Ghaedi [Iran]Source :
- Frontiers in oncology [ 2234-943X ] ; 2020.
Abstract
Receptor for advanced glycation end-products (RAGE) is a multiligand binding and single-pass transmembrane protein taken in diverse chronic inflammatory conditions. RAGE behaves as a pattern recognition receptor, which binds and is engaged in the cellular response to a variety of damage-associated molecular pattern molecules, as well as HMGB1, S100 proteins, and AGEs (advanced glycation end-products). The RAGE activation turns out to a formation of numerous intracellular signaling mechanisms, resulting in the progression and prolongation of colorectal carcinoma (CRC). The RAGE expression correlates well with the survival of colon cancer cells. RAGE is involved in the tumorigenesis, which increases and develops well in the stressed tumor microenvironment. In this review, we summarized downstream signaling cascade activated by the multiligand activation of RAGE, as well as RAGE ligands and their sources, clinical studies, and tumor markers related to RAGE particularly in the inflammatory tumor microenvironment in CRC. Furthermore, the role of RAGE signaling pathway in CRC patients with diabetic mellitus is investigated. RAGE has been reported to drive assorted signaling pathways, including activator protein 1, nuclear factor-κB, signal transducer and activator of transcription 3, SMAD family member 4 (Smad4), mitogen-activated protein kinases, mammalian target of rapamycin, phosphoinositide 3-kinases, reticular activating system, Wnt/β-catenin pathway, and Glycogen synthase kinase 3β, and even microRNAs.
DOI: 10.3389/fonc.2020.552283
PubMed: 33117687
PubMed Central: PMC7551201
Affiliations:
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wicri:step="Curation">000006</idno><idno type="wicri:Area/Main/Exploration">000006</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Receptor for Advanced Glycation End Products Acts as a Fuel to Colorectal Cancer Development.</title><author><name sortKey="Azizian Farsani, Fatemeh" sort="Azizian Farsani, Fatemeh" uniqKey="Azizian Farsani F" first="Fatemeh" last="Azizian-Farsani">Fatemeh Azizian-Farsani</name><affiliation wicri:level="1"><nlm:affiliation>Department of Medical Genetics, Shahid Sadoughi University of Medical Sciences, Yazd, Iran.</nlm:affiliation><country xml:lang="fr">Iran</country><wicri:regionArea>Department of Medical Genetics, Shahid Sadoughi University of Medical Sciences, Yazd</wicri:regionArea><wicri:noRegion>Yazd</wicri:noRegion></affiliation></author><author><name sortKey="Abedpoor, Navid" sort="Abedpoor, Navid" uniqKey="Abedpoor N" first="Navid" last="Abedpoor">Navid Abedpoor</name><affiliation wicri:level="1"><nlm:affiliation>Department of Animal Biotechnology, Cell Science Research Center, Royan Institute for Biotechnology, Academic Center for Education, Culture and Reasearch (ACECR), Isfahan, Iran.</nlm:affiliation><country xml:lang="fr">Iran</country><wicri:regionArea>Department of Animal Biotechnology, Cell Science Research Center, Royan Institute for Biotechnology, Academic Center for Education, Culture and Reasearch (ACECR), Isfahan</wicri:regionArea><wicri:noRegion>Isfahan</wicri:noRegion></affiliation></author><author><name sortKey="Hasan Sheikhha, Mohammad" sort="Hasan Sheikhha, Mohammad" uniqKey="Hasan Sheikhha M" first="Mohammad" last="Hasan Sheikhha">Mohammad Hasan Sheikhha</name><affiliation wicri:level="1"><nlm:affiliation>Department of Medical Genetics, Shahid Sadoughi University of Medical Sciences, Yazd, Iran.</nlm:affiliation><country xml:lang="fr">Iran</country><wicri:regionArea>Department of Medical Genetics, Shahid Sadoughi University of Medical Sciences, Yazd</wicri:regionArea><wicri:noRegion>Yazd</wicri:noRegion></affiliation></author><author><name sortKey="Gure, Ali Osmay" sort="Gure, Ali Osmay" uniqKey="Gure A" first="Ali Osmay" last="Gure">Ali Osmay Gure</name><affiliation wicri:level="1"><nlm:affiliation>Department of Molecular Biology and Genetics, Faculty of Science, Bilkent University, Ankara, Turkey.</nlm:affiliation><country xml:lang="fr">Turquie</country><wicri:regionArea>Department of Molecular Biology and Genetics, Faculty of Science, Bilkent University, Ankara</wicri:regionArea><wicri:noRegion>Ankara</wicri:noRegion></affiliation></author><author><name sortKey="Nasr Esfahani, Mohammad Hossein" sort="Nasr Esfahani, Mohammad Hossein" uniqKey="Nasr Esfahani M" first="Mohammad Hossein" last="Nasr-Esfahani">Mohammad Hossein Nasr-Esfahani</name><affiliation wicri:level="1"><nlm:affiliation>Department of Animal Biotechnology, Cell Science Research Center, Royan Institute for Biotechnology, Academic Center for Education, Culture and Reasearch (ACECR), Isfahan, Iran.</nlm:affiliation><country xml:lang="fr">Iran</country><wicri:regionArea>Department of Animal Biotechnology, Cell Science Research Center, Royan Institute for Biotechnology, Academic Center for Education, Culture and Reasearch (ACECR), Isfahan</wicri:regionArea><wicri:noRegion>Isfahan</wicri:noRegion></affiliation></author><author><name sortKey="Ghaedi, Kamran" sort="Ghaedi, Kamran" uniqKey="Ghaedi K" first="Kamran" last="Ghaedi">Kamran Ghaedi</name><affiliation wicri:level="1"><nlm:affiliation>Department of Animal Biotechnology, Cell Science Research Center, Royan Institute for Biotechnology, Academic Center for Education, Culture and Reasearch (ACECR), Isfahan, Iran.</nlm:affiliation><country xml:lang="fr">Iran</country><wicri:regionArea>Department of Animal Biotechnology, Cell Science Research Center, Royan Institute for Biotechnology, Academic Center for Education, Culture and Reasearch (ACECR), Isfahan</wicri:regionArea><wicri:noRegion>Isfahan</wicri:noRegion></affiliation><affiliation wicri:level="1"><nlm:affiliation>Division of Cellular and Molecular Biology, Department of Cell and Molecular Biology and Microbiology, Faculty of Biological Science and Technology, University of Isfahan, Isfahan, Iran.</nlm:affiliation><country xml:lang="fr">Iran</country><wicri:regionArea>Division of Cellular and Molecular Biology, Department of Cell and Molecular Biology and Microbiology, Faculty of Biological Science and Technology, University of Isfahan, Isfahan</wicri:regionArea><wicri:noRegion>Isfahan</wicri:noRegion></affiliation></author></analytic><series><title level="j">Frontiers in oncology</title><idno type="ISSN">2234-943X</idno><imprint><date when="2020" type="published">2020</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Receptor for advanced glycation end-products (RAGE) is a multiligand binding and single-pass transmembrane protein taken in diverse chronic inflammatory conditions. RAGE behaves as a pattern recognition receptor, which binds and is engaged in the cellular response to a variety of damage-associated molecular pattern molecules, as well as HMGB1, S100 proteins, and AGEs (advanced glycation end-products). The RAGE activation turns out to a formation of numerous intracellular signaling mechanisms, resulting in the progression and prolongation of colorectal carcinoma (CRC). The RAGE expression correlates well with the survival of colon cancer cells. RAGE is involved in the tumorigenesis, which increases and develops well in the stressed tumor microenvironment. In this review, we summarized downstream signaling cascade activated by the multiligand activation of RAGE, as well as RAGE ligands and their sources, clinical studies, and tumor markers related to RAGE particularly in the inflammatory tumor microenvironment in CRC. Furthermore, the role of RAGE signaling pathway in CRC patients with diabetic mellitus is investigated. RAGE has been reported to drive assorted signaling pathways, including activator protein 1, nuclear factor-κB, signal transducer and activator of transcription 3, SMAD family member 4 (Smad4), mitogen-activated protein kinases, mammalian target of rapamycin, phosphoinositide 3-kinases, reticular activating system, Wnt/β-catenin pathway, and Glycogen synthase kinase 3β, and even microRNAs.</div></front></TEI><pubmed><MedlineCitation Status="PubMed-not-MEDLINE" Owner="NLM"><PMID Version="1">33117687</PMID><DateRevised><Year>2020</Year><Month>10</Month><Day>30</Day></DateRevised><Article PubModel="Electronic-eCollection"><Journal><ISSN IssnType="Print">2234-943X</ISSN><JournalIssue CitedMedium="Print"><Volume>10</Volume><PubDate><Year>2020</Year></PubDate></JournalIssue><Title>Frontiers in oncology</Title><ISOAbbreviation>Front Oncol</ISOAbbreviation></Journal><ArticleTitle>Receptor for Advanced Glycation End Products Acts as a Fuel to Colorectal Cancer Development.</ArticleTitle><Pagination><MedlinePgn>552283</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.3389/fonc.2020.552283</ELocationID><Abstract><AbstractText>Receptor for advanced glycation end-products (RAGE) is a multiligand binding and single-pass transmembrane protein taken in diverse chronic inflammatory conditions. RAGE behaves as a pattern recognition receptor, which binds and is engaged in the cellular response to a variety of damage-associated molecular pattern molecules, as well as HMGB1, S100 proteins, and AGEs (advanced glycation end-products). The RAGE activation turns out to a formation of numerous intracellular signaling mechanisms, resulting in the progression and prolongation of colorectal carcinoma (CRC). The RAGE expression correlates well with the survival of colon cancer cells. RAGE is involved in the tumorigenesis, which increases and develops well in the stressed tumor microenvironment. In this review, we summarized downstream signaling cascade activated by the multiligand activation of RAGE, as well as RAGE ligands and their sources, clinical studies, and tumor markers related to RAGE particularly in the inflammatory tumor microenvironment in CRC. Furthermore, the role of RAGE signaling pathway in CRC patients with diabetic mellitus is investigated. RAGE has been reported to drive assorted signaling pathways, including activator protein 1, nuclear factor-κB, signal transducer and activator of transcription 3, SMAD family member 4 (Smad4), mitogen-activated protein kinases, mammalian target of rapamycin, phosphoinositide 3-kinases, reticular activating system, Wnt/β-catenin pathway, and Glycogen synthase kinase 3β, and even microRNAs.</AbstractText><CopyrightInformation>Copyright © 2020 Azizian-Farsani, Abedpoor, Hasan Sheikhha, Gure, Nasr-Esfahani and Ghaedi.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Azizian-Farsani</LastName><ForeName>Fatemeh</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>Department of Medical Genetics, Shahid Sadoughi University of Medical Sciences, Yazd, Iran.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Abedpoor</LastName><ForeName>Navid</ForeName><Initials>N</Initials><AffiliationInfo><Affiliation>Department of Animal Biotechnology, Cell Science Research Center, Royan Institute for Biotechnology, Academic Center for Education, Culture and Reasearch (ACECR), Isfahan, Iran.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hasan Sheikhha</LastName><ForeName>Mohammad</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Medical Genetics, Shahid Sadoughi University of Medical Sciences, Yazd, Iran.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gure</LastName><ForeName>Ali Osmay</ForeName><Initials>AO</Initials><AffiliationInfo><Affiliation>Department of Molecular Biology and Genetics, Faculty of Science, Bilkent University, Ankara, Turkey.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Nasr-Esfahani</LastName><ForeName>Mohammad Hossein</ForeName><Initials>MH</Initials><AffiliationInfo><Affiliation>Department of Animal Biotechnology, Cell Science Research Center, Royan Institute for Biotechnology, Academic Center for Education, Culture and Reasearch (ACECR), Isfahan, Iran.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ghaedi</LastName><ForeName>Kamran</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Department of Animal Biotechnology, Cell Science Research Center, Royan Institute for Biotechnology, Academic Center for Education, Culture and Reasearch (ACECR), Isfahan, Iran.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Division of Cellular and Molecular Biology, Department of Cell and Molecular Biology and Microbiology, Faculty of Biological Science and Technology, University of Isfahan, Isfahan, Iran.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2020</Year><Month>09</Month><Day>29</Day></ArticleDate></Article><MedlineJournalInfo><Country>Switzerland</Country><MedlineTA>Front Oncol</MedlineTA><NlmUniqueID>101568867</NlmUniqueID><ISSNLinking>2234-943X</ISSNLinking></MedlineJournalInfo><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">AGEs</Keyword><Keyword MajorTopicYN="N">CRC</Keyword><Keyword MajorTopicYN="N">RAGE (receptor for advanced glycation end products)</Keyword><Keyword MajorTopicYN="N">advanced glycation end products</Keyword><Keyword MajorTopicYN="N">colorectal cancer</Keyword><Keyword MajorTopicYN="N">damage-associated molecular pattern molecules (DAMPs)</Keyword><Keyword MajorTopicYN="N">pattern recognition receptor (PRR)</Keyword><Keyword MajorTopicYN="N">tumourogenesis</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2020</Year><Month>04</Month><Day>21</Day></PubMedPubDate><PubMedPubDate 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Kamran" sort="Ghaedi, Kamran" uniqKey="Ghaedi K" first="Kamran" last="Ghaedi">Kamran Ghaedi</name><name sortKey="Hasan Sheikhha, Mohammad" sort="Hasan Sheikhha, Mohammad" uniqKey="Hasan Sheikhha M" first="Mohammad" last="Hasan Sheikhha">Mohammad Hasan Sheikhha</name><name sortKey="Nasr Esfahani, Mohammad Hossein" sort="Nasr Esfahani, Mohammad Hossein" uniqKey="Nasr Esfahani M" first="Mohammad Hossein" last="Nasr-Esfahani">Mohammad Hossein Nasr-Esfahani</name></country><country name="Turquie"><noRegion><name sortKey="Gure, Ali Osmay" sort="Gure, Ali Osmay" uniqKey="Gure A" first="Ali Osmay" last="Gure">Ali Osmay Gure</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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