The up-regulated lncRNA DLX6-AS1 in colorectal cancer promotes cell proliferation, invasion and migration via modulating PI3K/AKT/mTOR pathway.
Identifieur interne : 000189 ( Main/Exploration ); précédent : 000188; suivant : 000190The up-regulated lncRNA DLX6-AS1 in colorectal cancer promotes cell proliferation, invasion and migration via modulating PI3K/AKT/mTOR pathway.
Auteurs : J-J Zhang [République populaire de Chine] ; W-R Xu ; B. Chen ; Y-Y Wang ; N. Yang ; L-J Wang ; Y-L ZhangSource :
- European review for medical and pharmacological sciences [ 2284-0729 ] ; 2019.
Descripteurs français
- KwdFr :
- Animaux (MeSH), Femelle (MeSH), Humains (MeSH), Invasion tumorale (MeSH), Lignée cellulaire tumorale (MeSH), Mouvement cellulaire (MeSH), Phosphatidylinositol 3-kinase (métabolisme), Prolifération cellulaire (MeSH), Protéine oncogène v-akt (métabolisme), Protéines à homéodomaine (métabolisme), Réaction de polymérisation en chaine en temps réel (MeSH), Régulation positive (MeSH), Souris nude (MeSH), Sérine-thréonine kinases TOR (métabolisme), Technique de Western (MeSH), Transduction du signal (MeSH), Transplantation tumorale (MeSH), Tumeurs colorectales (anatomopathologie), Tumeurs colorectales (métabolisme).
- MESH :
- anatomopathologie : Tumeurs colorectales.
- métabolisme : Phosphatidylinositol 3-kinase, Protéine oncogène v-akt, Protéines à homéodomaine, Sérine-thréonine kinases TOR, Tumeurs colorectales.
- Animaux, Femelle, Humains, Invasion tumorale, Lignée cellulaire tumorale, Mouvement cellulaire, Prolifération cellulaire, Réaction de polymérisation en chaine en temps réel, Régulation positive, Souris nude, Technique de Western, Transduction du signal, Transplantation tumorale.
English descriptors
- KwdEn :
- Animals (MeSH), Blotting, Western (MeSH), Cell Line, Tumor (MeSH), Cell Movement (MeSH), Cell Proliferation (MeSH), Colorectal Neoplasms (metabolism), Colorectal Neoplasms (pathology), Female (MeSH), Homeodomain Proteins (metabolism), Humans (MeSH), Mice, Nude (MeSH), Neoplasm Invasiveness (MeSH), Neoplasm Transplantation (MeSH), Oncogene Protein v-akt (metabolism), Phosphatidylinositol 3-Kinase (metabolism), Real-Time Polymerase Chain Reaction (MeSH), Signal Transduction (MeSH), TOR Serine-Threonine Kinases (metabolism), Up-Regulation (MeSH).
- MESH :
- chemical , metabolism : Homeodomain Proteins, Oncogene Protein v-akt, Phosphatidylinositol 3-Kinase, TOR Serine-Threonine Kinases.
- metabolism : Colorectal Neoplasms.
- pathology : Colorectal Neoplasms.
- Animals, Blotting, Western, Cell Line, Tumor, Cell Movement, Cell Proliferation, Female, Humans, Mice, Nude, Neoplasm Invasiveness, Neoplasm Transplantation, Real-Time Polymerase Chain Reaction, Signal Transduction, Up-Regulation.
Abstract
OBJECTIVE
Colorectal cancer (CRC) is one of the leading causes of cancer-related deaths around the world. Recently, using the high-throughput techniques, long non-coding RNAs (lncRNAs) have been shown to play an important role in CRC progression. In the present study, we aimed to determine lncRNA DLX6 Antisense RNA 1 (DLX6-AS1) in CRC tissues and cell lines and to investigate the molecular mechanisms of DLX6-AS1 in CRC progression.
PATIENTS AND METHODS
Quantitative real-time PCR was performed to detect gene expression; cell counting kit-8, colony formation, cell invasion, and migration assays were performed to determine cell proliferation, invasion, and migration, respectively; caspase-3 activity assay kit was used to detect caspase-3 activity; in vivo tumor growth was evaluated in a nude mice xenograft model.
RESULTS
DLX6-AS1 was up-regulated in 60 CRC tissues when compared to normal adjacent colorectal tissues, and high expression of DLX6-AS1 was correlated with advanced T stage and distant metastasis in CRC patients. The up-regulation of DLX6-AS1 was further confirmed in CRC cell lines. The gain-of-function assays showed that DLX6-AS1 overexpression promoted HCT116 cell proliferation, invasion, and migration, but inhibited cell apoptosis; while the loss-of-function assays showed that DLX6-AS1 knockdown exerted the opposite effects in SW480 cells. In vivo studies revealed that DLX6-AS1 knockdown suppressed tumor growth in the nude mice xenograft model. In addition, DLX6-AS1 overexpression caused an increase in the phosphorylated phosphoinositide 3-kinase (p-PI3K), p-AKT and p-mammalian target of rapamycin (mTOR) protein levels, and DLX6-AS1 knockdown had the opposite effects. Blockade of PI3K/AKT/mTOR signalling pathway by using mTOR inhibitor partially abolished the enhanced effects of DLX6-AS1 overexpression on CRC cell proliferation and metastasis.
CONCLUSIONS
In summary, our data indicated that DLX6-AS1 promoted CRC cell proliferation, invasion, and migration but inhibited cell apoptosis via targeting PI3K/AKT/mTOR signalling pathway, suggesting the key role of DLX6-AS1 in CRC progression.
DOI: 10.26355/eurrev_201910_19143
PubMed: 31646562
Affiliations:
Links toward previous steps (curation, corpus...)
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Chen</name></author><author><name sortKey="Wang, Y Y" sort="Wang, Y Y" uniqKey="Wang Y" first="Y-Y" last="Wang">Y-Y Wang</name></author><author><name sortKey="Yang, N" sort="Yang, N" uniqKey="Yang N" first="N" last="Yang">N. Yang</name></author><author><name sortKey="Wang, L J" sort="Wang, L J" uniqKey="Wang L" first="L-J" last="Wang">L-J Wang</name></author><author><name sortKey="Zhang, Y L" sort="Zhang, Y L" uniqKey="Zhang Y" first="Y-L" last="Zhang">Y-L Zhang</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2019">2019</date><idno type="RBID">pubmed:31646562</idno><idno type="pmid">31646562</idno><idno type="doi">10.26355/eurrev_201910_19143</idno><idno type="wicri:Area/Main/Corpus">000171</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Corpus" wicri:corpus="PubMed">000171</idno><idno type="wicri:Area/Main/Curation">000171</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Curation">000171</idno><idno type="wicri:Area/Main/Exploration">000171</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">The up-regulated lncRNA DLX6-AS1 in colorectal cancer promotes cell proliferation, invasion and migration via modulating PI3K/AKT/mTOR pathway.</title><author><name sortKey="Zhang, J J" sort="Zhang, J J" uniqKey="Zhang J" first="J-J" last="Zhang">J-J Zhang</name><affiliation wicri:level="1"><nlm:affiliation>Microbiology Laboratory, Xianyang Center for Disease Control and Prevention, Xianyang City, Shaanxi Province, China. zhangjunjun820122@163.com.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Microbiology Laboratory, Xianyang Center for Disease Control and Prevention, Xianyang City, Shaanxi Province</wicri:regionArea><wicri:noRegion>Shaanxi Province</wicri:noRegion></affiliation></author><author><name sortKey="Xu, W R" sort="Xu, W R" uniqKey="Xu W" first="W-R" last="Xu">W-R Xu</name></author><author><name sortKey="Chen, B" sort="Chen, B" uniqKey="Chen B" first="B" last="Chen">B. Chen</name></author><author><name sortKey="Wang, Y Y" sort="Wang, Y Y" uniqKey="Wang Y" first="Y-Y" last="Wang">Y-Y Wang</name></author><author><name sortKey="Yang, N" sort="Yang, N" uniqKey="Yang N" first="N" last="Yang">N. Yang</name></author><author><name sortKey="Wang, L J" sort="Wang, L J" uniqKey="Wang L" first="L-J" last="Wang">L-J Wang</name></author><author><name sortKey="Zhang, Y L" sort="Zhang, Y L" uniqKey="Zhang Y" first="Y-L" last="Zhang">Y-L Zhang</name></author></analytic><series><title level="j">European review for medical and pharmacological sciences</title><idno type="eISSN">2284-0729</idno><imprint><date when="2019" type="published">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term><term>Blotting, Western (MeSH)</term><term>Cell Line, Tumor (MeSH)</term><term>Cell Movement (MeSH)</term><term>Cell Proliferation (MeSH)</term><term>Colorectal Neoplasms (metabolism)</term><term>Colorectal Neoplasms (pathology)</term><term>Female (MeSH)</term><term>Homeodomain Proteins (metabolism)</term><term>Humans (MeSH)</term><term>Mice, Nude (MeSH)</term><term>Neoplasm Invasiveness (MeSH)</term><term>Neoplasm Transplantation (MeSH)</term><term>Oncogene Protein v-akt (metabolism)</term><term>Phosphatidylinositol 3-Kinase (metabolism)</term><term>Real-Time Polymerase Chain Reaction (MeSH)</term><term>Signal Transduction (MeSH)</term><term>TOR Serine-Threonine Kinases (metabolism)</term><term>Up-Regulation (MeSH)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux (MeSH)</term><term>Femelle (MeSH)</term><term>Humains (MeSH)</term><term>Invasion tumorale (MeSH)</term><term>Lignée cellulaire tumorale (MeSH)</term><term>Mouvement cellulaire (MeSH)</term><term>Phosphatidylinositol 3-kinase (métabolisme)</term><term>Prolifération cellulaire (MeSH)</term><term>Protéine oncogène v-akt (métabolisme)</term><term>Protéines à homéodomaine (métabolisme)</term><term>Réaction de polymérisation en chaine en temps réel (MeSH)</term><term>Régulation positive (MeSH)</term><term>Souris nude (MeSH)</term><term>Sérine-thréonine kinases TOR (métabolisme)</term><term>Technique de Western (MeSH)</term><term>Transduction du signal (MeSH)</term><term>Transplantation tumorale (MeSH)</term><term>Tumeurs colorectales (anatomopathologie)</term><term>Tumeurs colorectales (métabolisme)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Homeodomain Proteins</term><term>Oncogene Protein v-akt</term><term>Phosphatidylinositol 3-Kinase</term><term>TOR Serine-Threonine Kinases</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Tumeurs colorectales</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Colorectal Neoplasms</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Phosphatidylinositol 3-kinase</term><term>Protéine oncogène v-akt</term><term>Protéines à homéodomaine</term><term>Sérine-thréonine kinases TOR</term><term>Tumeurs colorectales</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Colorectal Neoplasms</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Blotting, Western</term><term>Cell Line, Tumor</term><term>Cell Movement</term><term>Cell Proliferation</term><term>Female</term><term>Humans</term><term>Mice, Nude</term><term>Neoplasm Invasiveness</term><term>Neoplasm Transplantation</term><term>Real-Time Polymerase Chain Reaction</term><term>Signal Transduction</term><term>Up-Regulation</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Femelle</term><term>Humains</term><term>Invasion tumorale</term><term>Lignée cellulaire tumorale</term><term>Mouvement cellulaire</term><term>Prolifération cellulaire</term><term>Réaction de polymérisation en chaine en temps réel</term><term>Régulation positive</term><term>Souris nude</term><term>Technique de Western</term><term>Transduction du signal</term><term>Transplantation tumorale</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p><b>OBJECTIVE</b></p><p>Colorectal cancer (CRC) is one of the leading causes of cancer-related deaths around the world. Recently, using the high-throughput techniques, long non-coding RNAs (lncRNAs) have been shown to play an important role in CRC progression. In the present study, we aimed to determine lncRNA DLX6 Antisense RNA 1 (DLX6-AS1) in CRC tissues and cell lines and to investigate the molecular mechanisms of DLX6-AS1 in CRC progression.</p></div><div type="abstract" xml:lang="en"><p><b>PATIENTS AND METHODS</b></p><p>Quantitative real-time PCR was performed to detect gene expression; cell counting kit-8, colony formation, cell invasion, and migration assays were performed to determine cell proliferation, invasion, and migration, respectively; caspase-3 activity assay kit was used to detect caspase-3 activity; in vivo tumor growth was evaluated in a nude mice xenograft model.</p></div><div type="abstract" xml:lang="en"><p><b>RESULTS</b></p><p>DLX6-AS1 was up-regulated in 60 CRC tissues when compared to normal adjacent colorectal tissues, and high expression of DLX6-AS1 was correlated with advanced T stage and distant metastasis in CRC patients. The up-regulation of DLX6-AS1 was further confirmed in CRC cell lines. The gain-of-function assays showed that DLX6-AS1 overexpression promoted HCT116 cell proliferation, invasion, and migration, but inhibited cell apoptosis; while the loss-of-function assays showed that DLX6-AS1 knockdown exerted the opposite effects in SW480 cells. In vivo studies revealed that DLX6-AS1 knockdown suppressed tumor growth in the nude mice xenograft model. In addition, DLX6-AS1 overexpression caused an increase in the phosphorylated phosphoinositide 3-kinase (p-PI3K), p-AKT and p-mammalian target of rapamycin (mTOR) protein levels, and DLX6-AS1 knockdown had the opposite effects. Blockade of PI3K/AKT/mTOR signalling pathway by using mTOR inhibitor partially abolished the enhanced effects of DLX6-AS1 overexpression on CRC cell proliferation and metastasis.</p></div><div type="abstract" xml:lang="en"><p><b>CONCLUSIONS</b></p><p>In summary, our data indicated that DLX6-AS1 promoted CRC cell proliferation, invasion, and migration but inhibited cell apoptosis via targeting PI3K/AKT/mTOR signalling pathway, suggesting the key role of DLX6-AS1 in CRC progression.</p></div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">31646562</PMID><DateCompleted><Year>2020</Year><Month>10</Month><Day>26</Day></DateCompleted><DateRevised><Year>2020</Year><Month>10</Month><Day>26</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">2284-0729</ISSN><JournalIssue CitedMedium="Internet"><Volume>23</Volume><Issue>19</Issue><PubDate><Year>2019</Year><Month>Oct</Month></PubDate></JournalIssue><Title>European review for medical and pharmacological sciences</Title><ISOAbbreviation>Eur Rev Med Pharmacol Sci</ISOAbbreviation></Journal><ArticleTitle>The up-regulated lncRNA DLX6-AS1 in colorectal cancer promotes cell proliferation, invasion and migration via modulating PI3K/AKT/mTOR pathway.</ArticleTitle><Pagination><MedlinePgn>8321-8331</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">19143</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.26355/eurrev_201910_19143</ELocationID><Abstract><AbstractText Label="OBJECTIVE" NlmCategory="OBJECTIVE">Colorectal cancer (CRC) is one of the leading causes of cancer-related deaths around the world. Recently, using the high-throughput techniques, long non-coding RNAs (lncRNAs) have been shown to play an important role in CRC progression. In the present study, we aimed to determine lncRNA DLX6 Antisense RNA 1 (DLX6-AS1) in CRC tissues and cell lines and to investigate the molecular mechanisms of DLX6-AS1 in CRC progression.</AbstractText><AbstractText Label="PATIENTS AND METHODS" NlmCategory="METHODS">Quantitative real-time PCR was performed to detect gene expression; cell counting kit-8, colony formation, cell invasion, and migration assays were performed to determine cell proliferation, invasion, and migration, respectively; caspase-3 activity assay kit was used to detect caspase-3 activity; in vivo tumor growth was evaluated in a nude mice xenograft model.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">DLX6-AS1 was up-regulated in 60 CRC tissues when compared to normal adjacent colorectal tissues, and high expression of DLX6-AS1 was correlated with advanced T stage and distant metastasis in CRC patients. The up-regulation of DLX6-AS1 was further confirmed in CRC cell lines. The gain-of-function assays showed that DLX6-AS1 overexpression promoted HCT116 cell proliferation, invasion, and migration, but inhibited cell apoptosis; while the loss-of-function assays showed that DLX6-AS1 knockdown exerted the opposite effects in SW480 cells. In vivo studies revealed that DLX6-AS1 knockdown suppressed tumor growth in the nude mice xenograft model. In addition, DLX6-AS1 overexpression caused an increase in the phosphorylated phosphoinositide 3-kinase (p-PI3K), p-AKT and p-mammalian target of rapamycin (mTOR) protein levels, and DLX6-AS1 knockdown had the opposite effects. Blockade of PI3K/AKT/mTOR signalling pathway by using mTOR inhibitor partially abolished the enhanced effects of DLX6-AS1 overexpression on CRC cell proliferation and metastasis.</AbstractText><AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">In summary, our data indicated that DLX6-AS1 promoted CRC cell proliferation, invasion, and migration but inhibited cell apoptosis via targeting PI3K/AKT/mTOR signalling pathway, suggesting the key role of DLX6-AS1 in CRC progression.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>J-J</ForeName><Initials>JJ</Initials><AffiliationInfo><Affiliation>Microbiology Laboratory, Xianyang Center for Disease Control and Prevention, Xianyang City, Shaanxi Province, China. zhangjunjun820122@163.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Xu</LastName><ForeName>W-R</ForeName><Initials>WR</Initials></Author><Author ValidYN="Y"><LastName>Chen</LastName><ForeName>B</ForeName><Initials>B</Initials></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Y-Y</ForeName><Initials>YY</Initials></Author><Author ValidYN="Y"><LastName>Yang</LastName><ForeName>N</ForeName><Initials>N</Initials></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>L-J</ForeName><Initials>LJ</Initials></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Y-L</ForeName><Initials>YL</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>Italy</Country><MedlineTA>Eur Rev Med Pharmacol Sci</MedlineTA><NlmUniqueID>9717360</NlmUniqueID><ISSNLinking>1128-3602</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C491014">DLX6 protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018398">Homeodomain Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.1.1</RegistryNumber><NameOfSubstance UI="C546842">MTOR protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.1.1</RegistryNumber><NameOfSubstance UI="D058570">TOR Serine-Threonine Kinases</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.1.137</RegistryNumber><NameOfSubstance UI="D058539">Phosphatidylinositol 3-Kinase</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.11.1</RegistryNumber><NameOfSubstance UI="D051058">Oncogene Protein v-akt</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015153" MajorTopicYN="N">Blotting, Western</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D045744" MajorTopicYN="N">Cell Line, Tumor</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002465" MajorTopicYN="N">Cell Movement</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D049109" MajorTopicYN="N">Cell Proliferation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015179" MajorTopicYN="N">Colorectal Neoplasms</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018398" MajorTopicYN="N">Homeodomain Proteins</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008819" MajorTopicYN="N">Mice, Nude</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009361" MajorTopicYN="N">Neoplasm Invasiveness</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009368" MajorTopicYN="N">Neoplasm Transplantation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051058" MajorTopicYN="N">Oncogene Protein v-akt</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D058539" MajorTopicYN="N">Phosphatidylinositol 3-Kinase</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D060888" MajorTopicYN="N">Real-Time Polymerase Chain Reaction</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015398" MajorTopicYN="Y">Signal Transduction</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D058570" MajorTopicYN="N">TOR Serine-Threonine Kinases</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015854" MajorTopicYN="N">Up-Regulation</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2019</Year><Month>10</Month><Day>25</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2019</Year><Month>10</Month><Day>28</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2020</Year><Month>10</Month><Day>27</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">31646562</ArticleId><ArticleId IdType="doi">10.26355/eurrev_201910_19143</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>République populaire de Chine</li></country></list><tree><noCountry><name sortKey="Chen, B" sort="Chen, B" uniqKey="Chen B" first="B" last="Chen">B. Chen</name><name sortKey="Wang, L J" sort="Wang, L J" uniqKey="Wang L" first="L-J" last="Wang">L-J Wang</name><name sortKey="Wang, Y Y" sort="Wang, Y Y" uniqKey="Wang Y" first="Y-Y" last="Wang">Y-Y Wang</name><name sortKey="Xu, W R" sort="Xu, W R" uniqKey="Xu W" first="W-R" last="Xu">W-R Xu</name><name sortKey="Yang, N" sort="Yang, N" uniqKey="Yang N" first="N" last="Yang">N. Yang</name><name sortKey="Zhang, Y L" sort="Zhang, Y L" uniqKey="Zhang Y" first="Y-L" last="Zhang">Y-L Zhang</name></noCountry><country name="République populaire de Chine"><noRegion><name sortKey="Zhang, J J" sort="Zhang, J J" uniqKey="Zhang J" first="J-J" last="Zhang">J-J Zhang</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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