Serveur d'exploration sur la rapamycine et les champignons

Attention, ce site est en cours de développement !
Attention, site généré par des moyens informatiques à partir de corpus bruts.
Les informations ne sont donc pas validées.

MicroRNA‑140 suppresses Helicobacter pylori‑positive gastric cancer growth by enhancing the antitumor immune response.

Identifieur interne : 000280 ( Main/Exploration ); précédent : 000279; suivant : 000281

MicroRNA‑140 suppresses Helicobacter pylori‑positive gastric cancer growth by enhancing the antitumor immune response.

Auteurs : Min Zhao [République populaire de Chine] ; Qian Liu [République populaire de Chine] ; Wenxiang Liu [République populaire de Chine] ; He Zhou [République populaire de Chine] ; Xuan Zang [République populaire de Chine] ; Jiangyang Lu [République populaire de Chine]

Source :

RBID : pubmed:31322226

Descripteurs français

English descriptors

Abstract

Immune checkpoint blockade is a promising therapeutic strategy against various human malignancies. MicroRNAs (miRNAs/miRs) regulate gene expression, by repressing mRNA translation or promoting its degradation. The aim of the current study was to investigate the role and molecular mechanisms of miR‑140 in Helicobacter pylori (Hp)‑associated gastric cancer, and to examine its relationship with immune function in gastric cancer. Gastritis tissue samples from gastritis patients, and gastric cancer tissue samples from gastric cancer patients were collected for miR‑140 expression detection. miR‑140 expression was detected using reverse transcription‑quantitative polymerase chain reaction, and protein expression was measured by western blotting. TargetScan and dual luciferase reporter assays were used to reveal the association between miR‑140 and programmed cell death‑ligand 1 (PD‑L1). BGC823 cell proliferation was detected by MTT assays. Ex vivo immune analysis by flow cytometry and ELISA were used to analyze immune function. It was demonstrated that miR‑140 expression was significantly reduced in Hp‑positive gastric cancer. PD‑L1 was confirmed as a direct target of miR‑140 in gastric cancer cells. In addition, PD‑L1 expression was significantly increased in Hp‑positive gastric cancer. Overexpression of miR‑140 significantly suppressed gastric cancer cell proliferation through regulating PD‑L1 expression. In vivo experiments also revealed that miR‑140 markedly repressed tumor growth in the C57BL/6 mice. Furthermore, it was determined that the tumor‑suppressive role of miR‑140 in gastric cancer was associated with increased cytotoxic CD8+ T cell and reduced myeloid‑derived suppressive and regulatory T cell infiltration. miR‑140 significantly prevented mammalian target of rapamycin signaling in gastric cancer cells. Notably, these miR‑140 overexpression‑induced alterations were inhibited by PD‑L1 plasmid. These findings indicated that miR‑140 exerted an anti‑gastric cancer effect by targeting immune checkpoint molecule PD‑L1. Thus, miR‑140 may be a promising and novel immunotherapeutic target for gastric cancer treatment.

DOI: 10.3892/mmr.2019.10475
PubMed: 31322226


Affiliations:


Links toward previous steps (curation, corpus...)


Le document en format XML

<record>
<TEI>
<teiHeader>
<fileDesc>
<titleStmt>
<title xml:lang="en">MicroRNA‑140 suppresses Helicobacter pylori‑positive gastric cancer growth by enhancing the antitumor immune response.</title>
<author>
<name sortKey="Zhao, Min" sort="Zhao, Min" uniqKey="Zhao M" first="Min" last="Zhao">Min Zhao</name>
<affiliation wicri:level="1">
<nlm:affiliation>Department of Pathology, The First Affiliated Hospital of General Hospital of People's Liberation Army, Beijing 100048, P.R. China.</nlm:affiliation>
<country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country>
<wicri:regionArea>Department of Pathology, The First Affiliated Hospital of General Hospital of People's Liberation Army, Beijing 100048</wicri:regionArea>
<placeName>
<settlement type="city">Pékin</settlement>
</placeName>
</affiliation>
</author>
<author>
<name sortKey="Liu, Qian" sort="Liu, Qian" uniqKey="Liu Q" first="Qian" last="Liu">Qian Liu</name>
<affiliation wicri:level="1">
<nlm:affiliation>Department of Pathology, The First Affiliated Hospital of General Hospital of People's Liberation Army, Beijing 100048, P.R. China.</nlm:affiliation>
<country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country>
<wicri:regionArea>Department of Pathology, The First Affiliated Hospital of General Hospital of People's Liberation Army, Beijing 100048</wicri:regionArea>
<placeName>
<settlement type="city">Pékin</settlement>
</placeName>
</affiliation>
</author>
<author>
<name sortKey="Liu, Wenxiang" sort="Liu, Wenxiang" uniqKey="Liu W" first="Wenxiang" last="Liu">Wenxiang Liu</name>
<affiliation wicri:level="1">
<nlm:affiliation>Department of Pathology, The First Affiliated Hospital of General Hospital of People's Liberation Army, Beijing 100048, P.R. China.</nlm:affiliation>
<country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country>
<wicri:regionArea>Department of Pathology, The First Affiliated Hospital of General Hospital of People's Liberation Army, Beijing 100048</wicri:regionArea>
<placeName>
<settlement type="city">Pékin</settlement>
</placeName>
</affiliation>
</author>
<author>
<name sortKey="Zhou, He" sort="Zhou, He" uniqKey="Zhou H" first="He" last="Zhou">He Zhou</name>
<affiliation wicri:level="1">
<nlm:affiliation>Department of Pathology, The First Affiliated Hospital of General Hospital of People's Liberation Army, Beijing 100048, P.R. China.</nlm:affiliation>
<country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country>
<wicri:regionArea>Department of Pathology, The First Affiliated Hospital of General Hospital of People's Liberation Army, Beijing 100048</wicri:regionArea>
<placeName>
<settlement type="city">Pékin</settlement>
</placeName>
</affiliation>
</author>
<author>
<name sortKey="Zang, Xuan" sort="Zang, Xuan" uniqKey="Zang X" first="Xuan" last="Zang">Xuan Zang</name>
<affiliation wicri:level="1">
<nlm:affiliation>Department of Pathology, The First Affiliated Hospital of General Hospital of People's Liberation Army, Beijing 100048, P.R. China.</nlm:affiliation>
<country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country>
<wicri:regionArea>Department of Pathology, The First Affiliated Hospital of General Hospital of People's Liberation Army, Beijing 100048</wicri:regionArea>
<placeName>
<settlement type="city">Pékin</settlement>
</placeName>
</affiliation>
</author>
<author>
<name sortKey="Lu, Jiangyang" sort="Lu, Jiangyang" uniqKey="Lu J" first="Jiangyang" last="Lu">Jiangyang Lu</name>
<affiliation wicri:level="1">
<nlm:affiliation>Department of Pathology, The First Affiliated Hospital of General Hospital of People's Liberation Army, Beijing 100048, P.R. China.</nlm:affiliation>
<country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country>
<wicri:regionArea>Department of Pathology, The First Affiliated Hospital of General Hospital of People's Liberation Army, Beijing 100048</wicri:regionArea>
<placeName>
<settlement type="city">Pékin</settlement>
</placeName>
</affiliation>
</author>
</titleStmt>
<publicationStmt>
<idno type="wicri:source">PubMed</idno>
<date when="2019">2019</date>
<idno type="RBID">pubmed:31322226</idno>
<idno type="pmid">31322226</idno>
<idno type="doi">10.3892/mmr.2019.10475</idno>
<idno type="wicri:Area/Main/Corpus">000230</idno>
<idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Corpus" wicri:corpus="PubMed">000230</idno>
<idno type="wicri:Area/Main/Curation">000230</idno>
<idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Curation">000230</idno>
<idno type="wicri:Area/Main/Exploration">000230</idno>
</publicationStmt>
<sourceDesc>
<biblStruct>
<analytic>
<title xml:lang="en">MicroRNA‑140 suppresses Helicobacter pylori‑positive gastric cancer growth by enhancing the antitumor immune response.</title>
<author>
<name sortKey="Zhao, Min" sort="Zhao, Min" uniqKey="Zhao M" first="Min" last="Zhao">Min Zhao</name>
<affiliation wicri:level="1">
<nlm:affiliation>Department of Pathology, The First Affiliated Hospital of General Hospital of People's Liberation Army, Beijing 100048, P.R. China.</nlm:affiliation>
<country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country>
<wicri:regionArea>Department of Pathology, The First Affiliated Hospital of General Hospital of People's Liberation Army, Beijing 100048</wicri:regionArea>
<placeName>
<settlement type="city">Pékin</settlement>
</placeName>
</affiliation>
</author>
<author>
<name sortKey="Liu, Qian" sort="Liu, Qian" uniqKey="Liu Q" first="Qian" last="Liu">Qian Liu</name>
<affiliation wicri:level="1">
<nlm:affiliation>Department of Pathology, The First Affiliated Hospital of General Hospital of People's Liberation Army, Beijing 100048, P.R. China.</nlm:affiliation>
<country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country>
<wicri:regionArea>Department of Pathology, The First Affiliated Hospital of General Hospital of People's Liberation Army, Beijing 100048</wicri:regionArea>
<placeName>
<settlement type="city">Pékin</settlement>
</placeName>
</affiliation>
</author>
<author>
<name sortKey="Liu, Wenxiang" sort="Liu, Wenxiang" uniqKey="Liu W" first="Wenxiang" last="Liu">Wenxiang Liu</name>
<affiliation wicri:level="1">
<nlm:affiliation>Department of Pathology, The First Affiliated Hospital of General Hospital of People's Liberation Army, Beijing 100048, P.R. China.</nlm:affiliation>
<country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country>
<wicri:regionArea>Department of Pathology, The First Affiliated Hospital of General Hospital of People's Liberation Army, Beijing 100048</wicri:regionArea>
<placeName>
<settlement type="city">Pékin</settlement>
</placeName>
</affiliation>
</author>
<author>
<name sortKey="Zhou, He" sort="Zhou, He" uniqKey="Zhou H" first="He" last="Zhou">He Zhou</name>
<affiliation wicri:level="1">
<nlm:affiliation>Department of Pathology, The First Affiliated Hospital of General Hospital of People's Liberation Army, Beijing 100048, P.R. China.</nlm:affiliation>
<country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country>
<wicri:regionArea>Department of Pathology, The First Affiliated Hospital of General Hospital of People's Liberation Army, Beijing 100048</wicri:regionArea>
<placeName>
<settlement type="city">Pékin</settlement>
</placeName>
</affiliation>
</author>
<author>
<name sortKey="Zang, Xuan" sort="Zang, Xuan" uniqKey="Zang X" first="Xuan" last="Zang">Xuan Zang</name>
<affiliation wicri:level="1">
<nlm:affiliation>Department of Pathology, The First Affiliated Hospital of General Hospital of People's Liberation Army, Beijing 100048, P.R. China.</nlm:affiliation>
<country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country>
<wicri:regionArea>Department of Pathology, The First Affiliated Hospital of General Hospital of People's Liberation Army, Beijing 100048</wicri:regionArea>
<placeName>
<settlement type="city">Pékin</settlement>
</placeName>
</affiliation>
</author>
<author>
<name sortKey="Lu, Jiangyang" sort="Lu, Jiangyang" uniqKey="Lu J" first="Jiangyang" last="Lu">Jiangyang Lu</name>
<affiliation wicri:level="1">
<nlm:affiliation>Department of Pathology, The First Affiliated Hospital of General Hospital of People's Liberation Army, Beijing 100048, P.R. China.</nlm:affiliation>
<country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country>
<wicri:regionArea>Department of Pathology, The First Affiliated Hospital of General Hospital of People's Liberation Army, Beijing 100048</wicri:regionArea>
<placeName>
<settlement type="city">Pékin</settlement>
</placeName>
</affiliation>
</author>
</analytic>
<series>
<title level="j">Molecular medicine reports</title>
<idno type="eISSN">1791-3004</idno>
<imprint>
<date when="2019" type="published">2019</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
</fileDesc>
<profileDesc>
<textClass>
<keywords scheme="KwdEn" xml:lang="en">
<term>Adult (MeSH)</term>
<term>Animals (MeSH)</term>
<term>B7-H1 Antigen (genetics)</term>
<term>Cell Line, Tumor (MeSH)</term>
<term>Cell Proliferation (MeSH)</term>
<term>Female (MeSH)</term>
<term>Gene Expression Regulation, Neoplastic (MeSH)</term>
<term>Helicobacter Infections (complications)</term>
<term>Helicobacter Infections (genetics)</term>
<term>Helicobacter pylori (isolation & purification)</term>
<term>Humans (MeSH)</term>
<term>Male (MeSH)</term>
<term>Mice, Inbred C57BL (MeSH)</term>
<term>MicroRNAs (genetics)</term>
<term>Middle Aged (MeSH)</term>
<term>Stomach Neoplasms (genetics)</term>
<term>Stomach Neoplasms (virology)</term>
<term>Young Adult (MeSH)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr">
<term>Adulte (MeSH)</term>
<term>Adulte d'âge moyen (MeSH)</term>
<term>Animaux (MeSH)</term>
<term>Antigène CD274 (génétique)</term>
<term>Femelle (MeSH)</term>
<term>Helicobacter pylori (isolement et purification)</term>
<term>Humains (MeSH)</term>
<term>Infections à Helicobacter (complications)</term>
<term>Infections à Helicobacter (génétique)</term>
<term>Jeune adulte (MeSH)</term>
<term>Lignée cellulaire tumorale (MeSH)</term>
<term>Mâle (MeSH)</term>
<term>Prolifération cellulaire (MeSH)</term>
<term>Régulation de l'expression des gènes tumoraux (MeSH)</term>
<term>Souris de lignée C57BL (MeSH)</term>
<term>Tumeurs de l'estomac (génétique)</term>
<term>Tumeurs de l'estomac (virologie)</term>
<term>microARN (génétique)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en">
<term>B7-H1 Antigen</term>
<term>MicroRNAs</term>
</keywords>
<keywords scheme="MESH" qualifier="complications" xml:lang="en">
<term>Helicobacter Infections</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en">
<term>Helicobacter Infections</term>
<term>Stomach Neoplasms</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr">
<term>Antigène CD274</term>
<term>Infections à Helicobacter</term>
<term>Tumeurs de l'estomac</term>
<term>microARN</term>
</keywords>
<keywords scheme="MESH" qualifier="isolation & purification" xml:lang="en">
<term>Helicobacter pylori</term>
</keywords>
<keywords scheme="MESH" qualifier="isolement et purification" xml:lang="fr">
<term>Helicobacter pylori</term>
</keywords>
<keywords scheme="MESH" qualifier="virologie" xml:lang="fr">
<term>Tumeurs de l'estomac</term>
</keywords>
<keywords scheme="MESH" qualifier="virology" xml:lang="en">
<term>Stomach Neoplasms</term>
</keywords>
<keywords scheme="MESH" xml:lang="en">
<term>Adult</term>
<term>Animals</term>
<term>Cell Line, Tumor</term>
<term>Cell Proliferation</term>
<term>Female</term>
<term>Gene Expression Regulation, Neoplastic</term>
<term>Humans</term>
<term>Male</term>
<term>Mice, Inbred C57BL</term>
<term>Middle Aged</term>
<term>Young Adult</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr">
<term>Adulte</term>
<term>Adulte d'âge moyen</term>
<term>Animaux</term>
<term>Femelle</term>
<term>Humains</term>
<term>Jeune adulte</term>
<term>Lignée cellulaire tumorale</term>
<term>Mâle</term>
<term>Prolifération cellulaire</term>
<term>Régulation de l'expression des gènes tumoraux</term>
<term>Souris de lignée C57BL</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front>
<div type="abstract" xml:lang="en">Immune checkpoint blockade is a promising therapeutic strategy against various human malignancies. MicroRNAs (miRNAs/miRs) regulate gene expression, by repressing mRNA translation or promoting its degradation. The aim of the current study was to investigate the role and molecular mechanisms of miR‑140 in Helicobacter pylori (Hp)‑associated gastric cancer, and to examine its relationship with immune function in gastric cancer. Gastritis tissue samples from gastritis patients, and gastric cancer tissue samples from gastric cancer patients were collected for miR‑140 expression detection. miR‑140 expression was detected using reverse transcription‑quantitative polymerase chain reaction, and protein expression was measured by western blotting. TargetScan and dual luciferase reporter assays were used to reveal the association between miR‑140 and programmed cell death‑ligand 1 (PD‑L1). BGC823 cell proliferation was detected by MTT assays. Ex vivo immune analysis by flow cytometry and ELISA were used to analyze immune function. It was demonstrated that miR‑140 expression was significantly reduced in Hp‑positive gastric cancer. PD‑L1 was confirmed as a direct target of miR‑140 in gastric cancer cells. In addition, PD‑L1 expression was significantly increased in Hp‑positive gastric cancer. Overexpression of miR‑140 significantly suppressed gastric cancer cell proliferation through regulating PD‑L1 expression. In vivo experiments also revealed that miR‑140 markedly repressed tumor growth in the C57BL/6 mice. Furthermore, it was determined that the tumor‑suppressive role of miR‑140 in gastric cancer was associated with increased cytotoxic CD8+ T cell and reduced myeloid‑derived suppressive and regulatory T cell infiltration. miR‑140 significantly prevented mammalian target of rapamycin signaling in gastric cancer cells. Notably, these miR‑140 overexpression‑induced alterations were inhibited by PD‑L1 plasmid. These findings indicated that miR‑140 exerted an anti‑gastric cancer effect by targeting immune checkpoint molecule PD‑L1. Thus, miR‑140 may be a promising and novel immunotherapeutic target for gastric cancer treatment.</div>
</front>
</TEI>
<pubmed>
<MedlineCitation Status="MEDLINE" Owner="NLM">
<PMID Version="1">31322226</PMID>
<DateCompleted>
<Year>2020</Year>
<Month>01</Month>
<Day>13</Day>
</DateCompleted>
<DateRevised>
<Year>2020</Year>
<Month>01</Month>
<Day>13</Day>
</DateRevised>
<Article PubModel="Print-Electronic">
<Journal>
<ISSN IssnType="Electronic">1791-3004</ISSN>
<JournalIssue CitedMedium="Internet">
<Volume>20</Volume>
<Issue>3</Issue>
<PubDate>
<Year>2019</Year>
<Month>Sep</Month>
</PubDate>
</JournalIssue>
<Title>Molecular medicine reports</Title>
<ISOAbbreviation>Mol Med Rep</ISOAbbreviation>
</Journal>
<ArticleTitle>MicroRNA‑140 suppresses Helicobacter pylori‑positive gastric cancer growth by enhancing the antitumor immune response.</ArticleTitle>
<Pagination>
<MedlinePgn>2484-2492</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.3892/mmr.2019.10475</ELocationID>
<Abstract>
<AbstractText>Immune checkpoint blockade is a promising therapeutic strategy against various human malignancies. MicroRNAs (miRNAs/miRs) regulate gene expression, by repressing mRNA translation or promoting its degradation. The aim of the current study was to investigate the role and molecular mechanisms of miR‑140 in Helicobacter pylori (Hp)‑associated gastric cancer, and to examine its relationship with immune function in gastric cancer. Gastritis tissue samples from gastritis patients, and gastric cancer tissue samples from gastric cancer patients were collected for miR‑140 expression detection. miR‑140 expression was detected using reverse transcription‑quantitative polymerase chain reaction, and protein expression was measured by western blotting. TargetScan and dual luciferase reporter assays were used to reveal the association between miR‑140 and programmed cell death‑ligand 1 (PD‑L1). BGC823 cell proliferation was detected by MTT assays. Ex vivo immune analysis by flow cytometry and ELISA were used to analyze immune function. It was demonstrated that miR‑140 expression was significantly reduced in Hp‑positive gastric cancer. PD‑L1 was confirmed as a direct target of miR‑140 in gastric cancer cells. In addition, PD‑L1 expression was significantly increased in Hp‑positive gastric cancer. Overexpression of miR‑140 significantly suppressed gastric cancer cell proliferation through regulating PD‑L1 expression. In vivo experiments also revealed that miR‑140 markedly repressed tumor growth in the C57BL/6 mice. Furthermore, it was determined that the tumor‑suppressive role of miR‑140 in gastric cancer was associated with increased cytotoxic CD8+ T cell and reduced myeloid‑derived suppressive and regulatory T cell infiltration. miR‑140 significantly prevented mammalian target of rapamycin signaling in gastric cancer cells. Notably, these miR‑140 overexpression‑induced alterations were inhibited by PD‑L1 plasmid. These findings indicated that miR‑140 exerted an anti‑gastric cancer effect by targeting immune checkpoint molecule PD‑L1. Thus, miR‑140 may be a promising and novel immunotherapeutic target for gastric cancer treatment.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y">
<Author ValidYN="Y">
<LastName>Zhao</LastName>
<ForeName>Min</ForeName>
<Initials>M</Initials>
<AffiliationInfo>
<Affiliation>Department of Pathology, The First Affiliated Hospital of General Hospital of People's Liberation Army, Beijing 100048, P.R. China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Liu</LastName>
<ForeName>Qian</ForeName>
<Initials>Q</Initials>
<AffiliationInfo>
<Affiliation>Department of Pathology, The First Affiliated Hospital of General Hospital of People's Liberation Army, Beijing 100048, P.R. China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Liu</LastName>
<ForeName>Wenxiang</ForeName>
<Initials>W</Initials>
<AffiliationInfo>
<Affiliation>Department of Pathology, The First Affiliated Hospital of General Hospital of People's Liberation Army, Beijing 100048, P.R. China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Zhou</LastName>
<ForeName>He</ForeName>
<Initials>H</Initials>
<AffiliationInfo>
<Affiliation>Department of Pathology, The First Affiliated Hospital of General Hospital of People's Liberation Army, Beijing 100048, P.R. China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Zang</LastName>
<ForeName>Xuan</ForeName>
<Initials>X</Initials>
<AffiliationInfo>
<Affiliation>Department of Pathology, The First Affiliated Hospital of General Hospital of People's Liberation Army, Beijing 100048, P.R. China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Lu</LastName>
<ForeName>Jiangyang</ForeName>
<Initials>J</Initials>
<AffiliationInfo>
<Affiliation>Department of Pathology, The First Affiliated Hospital of General Hospital of People's Liberation Army, Beijing 100048, P.R. China.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<PublicationTypeList>
<PublicationType UI="D016428">Journal Article</PublicationType>
</PublicationTypeList>
<ArticleDate DateType="Electronic">
<Year>2019</Year>
<Month>07</Month>
<Day>08</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo>
<Country>Greece</Country>
<MedlineTA>Mol Med Rep</MedlineTA>
<NlmUniqueID>101475259</NlmUniqueID>
<ISSNLinking>1791-2997</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList>
<Chemical>
<RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D060890">B7-H1 Antigen</NameOfSubstance>
</Chemical>
<Chemical>
<RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C423236">CD274 protein, human</NameOfSubstance>
</Chemical>
<Chemical>
<RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C547828">MIRN140 microRNA, mouse</NameOfSubstance>
</Chemical>
<Chemical>
<RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D035683">MicroRNAs</NameOfSubstance>
</Chemical>
<Chemical>
<RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C544302">Mirn140 microRNA, human</NameOfSubstance>
</Chemical>
</ChemicalList>
<CitationSubset>IM</CitationSubset>
<MeshHeadingList>
<MeshHeading>
<DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D060890" MajorTopicYN="N">B7-H1 Antigen</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D045744" MajorTopicYN="N">Cell Line, Tumor</DescriptorName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D049109" MajorTopicYN="N">Cell Proliferation</DescriptorName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D015972" MajorTopicYN="N">Gene Expression Regulation, Neoplastic</DescriptorName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D016481" MajorTopicYN="N">Helicobacter Infections</DescriptorName>
<QualifierName UI="Q000150" MajorTopicYN="Y">complications</QualifierName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D016480" MajorTopicYN="N">Helicobacter pylori</DescriptorName>
<QualifierName UI="Q000302" MajorTopicYN="N">isolation & purification</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D008810" MajorTopicYN="N">Mice, Inbred C57BL</DescriptorName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D035683" MajorTopicYN="N">MicroRNAs</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D013274" MajorTopicYN="N">Stomach Neoplasms</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
<QualifierName UI="Q000821" MajorTopicYN="Y">virology</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D055815" MajorTopicYN="N">Young Adult</DescriptorName>
</MeshHeading>
</MeshHeadingList>
</MedlineCitation>
<PubmedData>
<History>
<PubMedPubDate PubStatus="received">
<Year>2018</Year>
<Month>04</Month>
<Day>14</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="accepted">
<Year>2018</Year>
<Month>11</Month>
<Day>14</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="pubmed">
<Year>2019</Year>
<Month>7</Month>
<Day>20</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="medline">
<Year>2020</Year>
<Month>1</Month>
<Day>14</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="entrez">
<Year>2019</Year>
<Month>7</Month>
<Day>20</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
</History>
<PublicationStatus>ppublish</PublicationStatus>
<ArticleIdList>
<ArticleId IdType="pubmed">31322226</ArticleId>
<ArticleId IdType="doi">10.3892/mmr.2019.10475</ArticleId>
</ArticleIdList>
</PubmedData>
</pubmed>
<affiliations>
<list>
<country>
<li>République populaire de Chine</li>
</country>
<settlement>
<li>Pékin</li>
</settlement>
</list>
<tree>
<country name="République populaire de Chine">
<noRegion>
<name sortKey="Zhao, Min" sort="Zhao, Min" uniqKey="Zhao M" first="Min" last="Zhao">Min Zhao</name>
</noRegion>
<name sortKey="Liu, Qian" sort="Liu, Qian" uniqKey="Liu Q" first="Qian" last="Liu">Qian Liu</name>
<name sortKey="Liu, Wenxiang" sort="Liu, Wenxiang" uniqKey="Liu W" first="Wenxiang" last="Liu">Wenxiang Liu</name>
<name sortKey="Lu, Jiangyang" sort="Lu, Jiangyang" uniqKey="Lu J" first="Jiangyang" last="Lu">Jiangyang Lu</name>
<name sortKey="Zang, Xuan" sort="Zang, Xuan" uniqKey="Zang X" first="Xuan" last="Zang">Xuan Zang</name>
<name sortKey="Zhou, He" sort="Zhou, He" uniqKey="Zhou H" first="He" last="Zhou">He Zhou</name>
</country>
</tree>
</affiliations>
</record>

Pour manipuler ce document sous Unix (Dilib)

EXPLOR_STEP=$WICRI_ROOT/Bois/explor/RapamycinFungusV1/Data/Main/Exploration
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000280 | SxmlIndent | more

Ou

HfdSelect -h $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd -nk 000280 | SxmlIndent | more

Pour mettre un lien sur cette page dans le réseau Wicri

{{Explor lien
   |wiki=    Bois
   |area=    RapamycinFungusV1
   |flux=    Main
   |étape=   Exploration
   |type=    RBID
   |clé=     pubmed:31322226
   |texte=   MicroRNA‑140 suppresses Helicobacter pylori‑positive gastric cancer growth by enhancing the antitumor immune response.
}}

Pour générer des pages wiki

HfdIndexSelect -h $EXPLOR_AREA/Data/Main/Exploration/RBID.i   -Sk "pubmed:31322226" \
       | HfdSelect -Kh $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd   \
       | NlmPubMed2Wicri -a RapamycinFungusV1 

Wicri

This area was generated with Dilib version V0.6.38.
Data generation: Thu Nov 19 21:55:41 2020. Site generation: Thu Nov 19 22:00:39 2020