Ortho-Topolin Riboside Induced Differentiation through Inhibition of STAT3 Signaling in Acute Myeloid Leukemia HL-60 Cells
Identifieur interne : 000811 ( Main/Exploration ); précédent : 000810; suivant : 000812Ortho-Topolin Riboside Induced Differentiation through Inhibition of STAT3 Signaling in Acute Myeloid Leukemia HL-60 Cells
Auteurs : Li Wang [République populaire de Chine] ; Jiao Cheng [République populaire de Chine] ; Fanlin Lin [République populaire de Chine] ; Shengxian Liu [République populaire de Chine] ; Hui Pan [République populaire de Chine] ; Mingda Li [République populaire de Chine] ; Shanshan Li [République populaire de Chine] ; Na Li [République populaire de Chine] ; Weiping Li [République populaire de Chine]Source :
- Turkish journal of haematology : official journal of Turkish Society of Haematology [ 1308-5263 ] ; 2019.
Descripteurs français
- KwdFr :
- MESH :
- anatomopathologie : Leucémie aigüe myéloïde.
- génétique : Leucémie aigüe myéloïde.
- pharmacologie : Cytokinine.
- usage thérapeutique : Cytokinine.
- Cellules HL-60, Différenciation cellulaire, Facteur de transcription STAT-3, Humains, Transduction du signal.
English descriptors
- KwdEn :
- MESH :
- chemical , pharmacology : Cytokinins.
- chemical , therapeutic use : Cytokinins.
- genetics : Leukemia, Myeloid, Acute.
- pathology : Leukemia, Myeloid, Acute.
- Cell Differentiation, HL-60 Cells, Humans, STAT3 Transcription Factor, Signal Transduction.
Abstract
Objective
We previously demonstrated that ortho-topolin riboside (oTR) as a naturally occurring cytokinin secreted from
Materials and Methods
After the incubation of HL-60 cells with oTR, its effect was analyzed with cell viability assay, Wright-Giemsa staining, CD11b protein expression analysis, western blot analysis, and polymerase chain reaction.
Results
We found that oTR arrested the cell cycle at the S phase, upregulated the expression of myeloid surface marker CD11b, reduced the nuclear cytoplasmic ratio, and altered the horseshoe shape of nuclei, as evidenced by Wright-Giemsa staining. Furthermore, we found that the protein level of phosphorylated STAT3 was decreased when cells were treated with oTR, while phosphorylated STAT1 was activated. Moreover, the protein level of phosphorylated STAT3 and its upstream kinase, Janus kinase 2, were also inhibited when cells were treated with oTR after increased time. Additionally, the levels of phosphorylated SHP-1 were increased while phosphorylated SHP-2 was decreased.
Conclusion
Collectively, our data indicate a differentiation-induced mechanism underlying the inhibition of STAT3 signaling upon treatment with oTR. Therefore, oTR may constitute a novel differentiation-induced therapeutic for use in clinical treatment of AML.
DOI: 10.4274/tjh.galenos.2019.2019.0020
PubMed: 31117333
PubMed Central: PMC6682775
Affiliations:
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Medicine, Dalian University of Technology, PanJin</wicri:regionArea><wicri:noRegion>PanJin</wicri:noRegion></affiliation></author><author><name sortKey="Li, Shanshan" sort="Li, Shanshan" uniqKey="Li S" first="Shanshan" last="Li">Shanshan Li</name><affiliation wicri:level="1"><nlm:affiliation>School of Life and Medicine, Dalian University of Technology, PanJin, China</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>School of Life and Medicine, Dalian University of Technology, PanJin</wicri:regionArea><wicri:noRegion>PanJin</wicri:noRegion></affiliation></author><author><name sortKey="Li, Na" sort="Li, Na" uniqKey="Li N" first="Na" last="Li">Na Li</name><affiliation wicri:level="1"><nlm:affiliation>The Second Hospital of Dalian Medical University, Dalian, China</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>The Second Hospital of Dalian Medical University, Dalian</wicri:regionArea><wicri:noRegion>Dalian</wicri:noRegion></affiliation></author><author><name sortKey="Li, Weiping" sort="Li, Weiping" uniqKey="Li W" first="Weiping" last="Li">Weiping Li</name><affiliation wicri:level="1"><nlm:affiliation>The Second Hospital of Dalian Medical University, Dalian, China</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>The Second Hospital of Dalian Medical University, Dalian</wicri:regionArea><wicri:noRegion>Dalian</wicri:noRegion></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2019">2019</date><idno type="RBID">pubmed:31117333</idno><idno type="pmid">31117333</idno><idno type="doi">10.4274/tjh.galenos.2019.2019.0020</idno><idno type="pmc">PMC6682775</idno><idno type="wicri:Area/Main/Corpus">000889</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Corpus" wicri:corpus="PubMed">000889</idno><idno 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wicri:level="1"><nlm:affiliation>School of Life and Medicine, Dalian University of Technology, PanJin, China</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>School of Life and Medicine, Dalian University of Technology, PanJin</wicri:regionArea><wicri:noRegion>PanJin</wicri:noRegion></affiliation></author><author><name sortKey="Lin, Fanlin" sort="Lin, Fanlin" uniqKey="Lin F" first="Fanlin" last="Lin">Fanlin Lin</name><affiliation wicri:level="1"><nlm:affiliation>School of Life and Medicine, Dalian University of Technology, PanJin, China</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>School of Life and Medicine, Dalian University of Technology, PanJin</wicri:regionArea><wicri:noRegion>PanJin</wicri:noRegion></affiliation></author><author><name sortKey="Liu, Shengxian" sort="Liu, Shengxian" uniqKey="Liu S" first="Shengxian" last="Liu">Shengxian Liu</name><affiliation wicri:level="1"><nlm:affiliation>School of Life and Medicine, Dalian University of Technology, PanJin, China</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>School of Life and Medicine, Dalian University of Technology, PanJin</wicri:regionArea><wicri:noRegion>PanJin</wicri:noRegion></affiliation></author><author><name sortKey="Pan, Hui" sort="Pan, Hui" uniqKey="Pan H" first="Hui" last="Pan">Hui Pan</name><affiliation wicri:level="1"><nlm:affiliation>School of Life and Medicine, Dalian University of Technology, PanJin, China</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>School of Life and Medicine, Dalian University of Technology, PanJin</wicri:regionArea><wicri:noRegion>PanJin</wicri:noRegion></affiliation></author><author><name sortKey="Li, Mingda" sort="Li, Mingda" uniqKey="Li M" first="Mingda" last="Li">Mingda Li</name><affiliation wicri:level="1"><nlm:affiliation>School of Life and Medicine, Dalian University of Technology, PanJin, China</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>School of Life and Medicine, Dalian University of Technology, PanJin</wicri:regionArea><wicri:noRegion>PanJin</wicri:noRegion></affiliation></author><author><name sortKey="Li, Shanshan" sort="Li, Shanshan" uniqKey="Li S" first="Shanshan" last="Li">Shanshan Li</name><affiliation wicri:level="1"><nlm:affiliation>School of Life and Medicine, Dalian University of Technology, PanJin, China</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>School of Life and Medicine, Dalian University of Technology, PanJin</wicri:regionArea><wicri:noRegion>PanJin</wicri:noRegion></affiliation></author><author><name sortKey="Li, Na" sort="Li, Na" uniqKey="Li N" first="Na" last="Li">Na Li</name><affiliation wicri:level="1"><nlm:affiliation>The Second Hospital of Dalian Medical University, Dalian, China</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>The Second Hospital of Dalian Medical University, Dalian</wicri:regionArea><wicri:noRegion>Dalian</wicri:noRegion></affiliation></author><author><name sortKey="Li, Weiping" sort="Li, Weiping" uniqKey="Li W" first="Weiping" last="Li">Weiping Li</name><affiliation wicri:level="1"><nlm:affiliation>The Second Hospital of Dalian Medical University, Dalian, China</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>The Second Hospital of Dalian Medical University, Dalian</wicri:regionArea><wicri:noRegion>Dalian</wicri:noRegion></affiliation></author></analytic><series><title level="j">Turkish journal of haematology : official journal of Turkish Society of Haematology</title><idno type="eISSN">1308-5263</idno><imprint><date when="2019" type="published">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Cell Differentiation (MeSH)</term><term>Cytokinins (pharmacology)</term><term>Cytokinins (therapeutic use)</term><term>HL-60 Cells (MeSH)</term><term>Humans (MeSH)</term><term>Leukemia, Myeloid, Acute (genetics)</term><term>Leukemia, Myeloid, Acute (pathology)</term><term>STAT3 Transcription Factor (MeSH)</term><term>Signal Transduction (MeSH)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Cellules HL-60 (MeSH)</term><term>Cytokinine (pharmacologie)</term><term>Cytokinine (usage thérapeutique)</term><term>Différenciation cellulaire (MeSH)</term><term>Facteur de transcription STAT-3 (MeSH)</term><term>Humains (MeSH)</term><term>Leucémie aigüe myéloïde (anatomopathologie)</term><term>Leucémie aigüe myéloïde (génétique)</term><term>Transduction du signal (MeSH)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Cytokinins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Cytokinins</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Leucémie aigüe myéloïde</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Leukemia, Myeloid, Acute</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Leucémie aigüe myéloïde</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Leukemia, Myeloid, Acute</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Cytokinine</term></keywords><keywords scheme="MESH" qualifier="usage thérapeutique" xml:lang="fr"><term>Cytokinine</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Cell Differentiation</term><term>HL-60 Cells</term><term>Humans</term><term>STAT3 Transcription Factor</term><term>Signal Transduction</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Cellules HL-60</term><term>Différenciation cellulaire</term><term>Facteur de transcription STAT-3</term><term>Humains</term><term>Transduction du signal</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p><b>Objective</b></p><p>We previously demonstrated that ortho-topolin riboside (oTR) as a naturally occurring cytokinin secreted from </p></div><div type="abstract" xml:lang="en"><p><b>Materials and Methods</b></p><p>After the incubation of HL-60 cells with oTR, its effect was analyzed with cell viability assay, Wright-Giemsa staining, CD11b protein expression analysis, western blot analysis, and polymerase chain reaction.</p></div><div type="abstract" xml:lang="en"><p><b>Results</b></p><p>We found that oTR arrested the cell cycle at the S phase, upregulated the expression of myeloid surface marker CD11b, reduced the nuclear cytoplasmic ratio, and altered the horseshoe shape of nuclei, as evidenced by Wright-Giemsa staining. Furthermore, we found that the protein level of phosphorylated STAT3 was decreased when cells were treated with oTR, while phosphorylated STAT1 was activated. Moreover, the protein level of phosphorylated STAT3 and its upstream kinase, Janus kinase 2, were also inhibited when cells were treated with oTR after increased time. Additionally, the levels of phosphorylated SHP-1 were increased while phosphorylated SHP-2 was decreased.</p></div><div type="abstract" xml:lang="en"><p><b>Conclusion</b></p><p>Collectively, our data indicate a differentiation-induced mechanism underlying the inhibition of STAT3 signaling upon treatment with oTR. Therefore, oTR may constitute a novel differentiation-induced therapeutic for use in clinical treatment of AML.</p></div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">31117333</PMID><DateCompleted><Year>2020</Year><Month>01</Month><Day>08</Day></DateCompleted><DateRevised><Year>2020</Year><Month>02</Month><Day>25</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1308-5263</ISSN><JournalIssue CitedMedium="Internet"><Volume>36</Volume><Issue>3</Issue><PubDate><Year>2019</Year><Month>08</Month><Day>02</Day></PubDate></JournalIssue><Title>Turkish journal of haematology : official journal of Turkish Society of Haematology</Title><ISOAbbreviation>Turk J Haematol</ISOAbbreviation></Journal><ArticleTitle>Ortho-Topolin Riboside Induced Differentiation through Inhibition of STAT3 Signaling in Acute Myeloid Leukemia HL-60 Cells</ArticleTitle><Pagination><MedlinePgn>162-168</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.4274/tjh.galenos.2019.2019.0020</ELocationID><Abstract><AbstractText Label="Objective">We previously demonstrated that ortho-topolin riboside (oTR) as a naturally occurring cytokinin secreted from <i>Populus</i> × <i>robusta</i> has great potential anticancer effects via the mitochondrial apoptotic pathway and endoplasmic reticulum stress pathway. In the present study, we reveal that oTR induced the differentiation of acute myeloid leukemia (AML) HL-60 cells, which represent the M2 subtype of AML.</AbstractText><AbstractText Label="Materials and Methods">After the incubation of HL-60 cells with oTR, its effect was analyzed with cell viability assay, Wright-Giemsa staining, CD11b protein expression analysis, western blot analysis, and polymerase chain reaction.</AbstractText><AbstractText Label="Results">We found that oTR arrested the cell cycle at the S phase, upregulated the expression of myeloid surface marker CD11b, reduced the nuclear cytoplasmic ratio, and altered the horseshoe shape of nuclei, as evidenced by Wright-Giemsa staining. Furthermore, we found that the protein level of phosphorylated STAT3 was decreased when cells were treated with oTR, while phosphorylated STAT1 was activated. Moreover, the protein level of phosphorylated STAT3 and its upstream kinase, Janus kinase 2, were also inhibited when cells were treated with oTR after increased time. Additionally, the levels of phosphorylated SHP-1 were increased while phosphorylated SHP-2 was decreased.</AbstractText><AbstractText Label="Conclusion">Collectively, our data indicate a differentiation-induced mechanism underlying the inhibition of STAT3 signaling upon treatment with oTR. Therefore, oTR may constitute a novel differentiation-induced therapeutic for use in clinical treatment of AML.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Li</ForeName><Initials>L</Initials><Identifier Source="ORCID">0000-0001-6567-2578</Identifier><AffiliationInfo><Affiliation>School of Life and Medicine, Dalian University of Technology, PanJin, China</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Cheng</LastName><ForeName>Jiao</ForeName><Initials>J</Initials><Identifier Source="ORCID">0000-0001-6050-4671</Identifier><AffiliationInfo><Affiliation>School of Life and Medicine, Dalian University of Technology, PanJin, China</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lin</LastName><ForeName>FanLin</ForeName><Initials>F</Initials><Identifier Source="ORCID">0000-0001-7797-7192</Identifier><AffiliationInfo><Affiliation>School of Life and Medicine, Dalian University of Technology, PanJin, China</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>ShengXian</ForeName><Initials>S</Initials><Identifier Source="ORCID">0000-0001-8371-2561</Identifier><AffiliationInfo><Affiliation>School of Life and Medicine, Dalian University of Technology, PanJin, China</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Pan</LastName><ForeName>Hui</ForeName><Initials>H</Initials><Identifier Source="ORCID">0000-0002-9907-600X</Identifier><AffiliationInfo><Affiliation>School of Life and Medicine, Dalian University of Technology, PanJin, China</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>MingDa</ForeName><Initials>M</Initials><Identifier Source="ORCID">0000-0001-5800-1303</Identifier><AffiliationInfo><Affiliation>School of Life and Medicine, Dalian University of Technology, PanJin, China</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>ShanShan</ForeName><Initials>S</Initials><Identifier Source="ORCID">0000-0003-4545-6442</Identifier><AffiliationInfo><Affiliation>School of Life and Medicine, Dalian University of Technology, PanJin, China</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Na</ForeName><Initials>N</Initials><Identifier Source="ORCID">0000-0001-5229-2787</Identifier><AffiliationInfo><Affiliation>The Second Hospital of Dalian Medical University, Dalian, China</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>WeiPing</ForeName><Initials>W</Initials><Identifier Source="ORCID">0000-0002-1843-9906</Identifier><AffiliationInfo><Affiliation>The Second Hospital of Dalian Medical University, Dalian, China</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2019</Year><Month>05</Month><Day>23</Day></ArticleDate></Article><MedlineJournalInfo><Country>Turkey</Country><MedlineTA>Turk J Haematol</MedlineTA><NlmUniqueID>9606065</NlmUniqueID><ISSNLinking>1300-7777</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D003583">Cytokinins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D050796">STAT3 Transcription Factor</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C494086">STAT3 protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C575434">ortho-topolin riboside</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D002454" MajorTopicYN="N">Cell Differentiation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003583" MajorTopicYN="N">Cytokinins</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName><QualifierName UI="Q000627" MajorTopicYN="Y">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018922" MajorTopicYN="N">HL-60 Cells</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015470" MajorTopicYN="N">Leukemia, Myeloid, Acute</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D050796" MajorTopicYN="N">STAT3 Transcription Factor</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName></MeshHeading></MeshHeadingList><OtherAbstract Type="Publisher" Language="tur"><AbstractText Label="Amaç">Daha önceki çalışmalarımızda <i>Populus</i> × <i>robusta</i>’dan doğal olarak oluşan sitokin orto-topolin ribozidin (oTR) mitokondrial apopitotik yolaklar ve endoplazmik retikulum stres yolakları vasıtasıyla önemli bir antikanser potansiyelinin olduğunu göstermiştik. Bu çalışmada, oTR’nin AML M2 subtipi özelliğindeki HL-60 hücre serisinde diferansiyasyonu indüklediğini gösterdik.</AbstractText><AbstractText Label="Gereç ve Yöntemler">HL-60 hücrelerinin oTR ile inkübasyonunu takiben hücre üzerideki etkileri hücre canlılık testleri, Wright-Giemsa boyaması, CD11b protein ekspresyon analizi, western blot analizi ve polimeraz zincir reaksiyonu ile araştırıldı.</AbstractText><AbstractText Label="Bulgular">oTR’nin hücre siklusunun S fazında duraklattığını, myeloid hücre yüzey belirteçlerinden CD11b ekspresyonunun arttığını, çekirdek sitoplazma oranının azaldığını ve çekirdeğin atnalı şeklinin değiştiğini Wright-Giemsa boyası ile destekleyerek gördük. oTR ile muamele edilmiş hücrelerde fosforile STAT3 protein düzeyinin azaldığını, fosforile STAT1’in ise aktive olduğunu bulduk. Ayrıca fosforile STAT3 ve yukarı yöndeki kinaz olan Janus kinaz 2’nin, hücrelerin oTR ile inkübasyonunda artmış zamanla inhibe olduğu görüldü. Ek olarak fosforile SHP-1 düzeyleri artarken fosforile SHP-2 düzeyi azaldı.</AbstractText><AbstractText Label="Sonuç">Birlikte değerlendirildiğinde, sonuçlarımız oTR ile STAT3 inhibisyonu üzerinden bir diferansiyasyon indükleme mekanizmasını işaret etmektedir. Bu nedenle, oTR AML tedavisinde yeni bir diferansiyasyon-indükleyici terapötik olarak yer alabilir.</AbstractText></OtherAbstract><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">Ortho-topolin riboside</Keyword><Keyword MajorTopicYN="Y">STAT3 signal</Keyword><Keyword MajorTopicYN="Y">HL-60 cells</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2019</Year><Month>5</Month><Day>24</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2019</Year><Month>5</Month><Day>24</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2020</Year><Month>1</Month><Day>9</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">31117333</ArticleId><ArticleId IdType="doi">10.4274/tjh.galenos.2019.2019.0020</ArticleId><ArticleId 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