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Mangiferin inhibits lipopolysaccharide-induced epithelial-mesenchymal transition (EMT) and enhances the expression of tumor suppressor gene PER1 in non-small cell lung cancer cells.

Identifieur interne : 000117 ( Main/Exploration ); précédent : 000116; suivant : 000118

Mangiferin inhibits lipopolysaccharide-induced epithelial-mesenchymal transition (EMT) and enhances the expression of tumor suppressor gene PER1 in non-small cell lung cancer cells.

Auteurs : Yen-Sung Lin [Taïwan] ; Kun-Ling Tsai [Taïwan] ; Jia-Ni Chen [Taïwan] ; Chen-Shiou Wu [Taïwan]

Source :

RBID : pubmed:32420661

Descripteurs français

English descriptors

Abstract

Non-small cell lung cancer (NSCLC) is often complicated by pulmonary infection, which affects treatment and prognosis. Bacterial lipopolysaccharide (LPS) is an effective stimulator of inflammatory cytokine production, and previous studies have reported that LPS promotes tumor invasion and metastasis. Mangiferin is a plant-derived C-glucosylxanthone with many biological activities, such as antioxidation and anti-inflammation. This research mainly explored the mechanism of its antitumor activities on LPS-induced A549, NCI-H460, and NCI-H520 NSCLC cells. We determined that mangiferin exhibits growth inhibiting activity against LPS-induced NSCLC cells through the 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assay. In addition, mangiferin reversed the LPS-induced downregulation of E-cadherin (epithelial marker); conversely, it significantly inhibited the expression of raised vimentin (mesenchymal markers). Moreover, the ability of NSCLC cells to migrate, as evidenced by the wound healing and transwell migration assays, and the expression of CXCR4 increased by LPS were significantly repressed by mangiferin. In addition, mangiferin markedly mediated protein levels of PER1 and NLRP3 in LPS-induced NSCLC cells and reduced the secretion of IL-1β. These results indicate that mangiferin is not only a remarkable anti-inflammatory compound but also an antitumor agent; thus, it has the potential for being developed into anti-inflammatory and antitumor drugs in the future.

DOI: 10.1002/tox.22943
PubMed: 32420661


Affiliations:


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Le document en format XML

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<term>A549 Cells (MeSH)</term>
<term>Antigens, CD (genetics)</term>
<term>Antineoplastic Agents, Phytogenic (pharmacology)</term>
<term>Cadherins (genetics)</term>
<term>Carcinoma, Non-Small-Cell Lung (genetics)</term>
<term>Carcinoma, Non-Small-Cell Lung (pathology)</term>
<term>Cell Line, Tumor (MeSH)</term>
<term>Cell Movement (drug effects)</term>
<term>Cell Movement (genetics)</term>
<term>Cell Proliferation (drug effects)</term>
<term>Cell Proliferation (genetics)</term>
<term>Down-Regulation (MeSH)</term>
<term>Epithelial-Mesenchymal Transition (drug effects)</term>
<term>Epithelial-Mesenchymal Transition (genetics)</term>
<term>Humans (MeSH)</term>
<term>Lipopolysaccharides (pharmacology)</term>
<term>Lung Neoplasms (genetics)</term>
<term>Lung Neoplasms (pathology)</term>
<term>Period Circadian Proteins (genetics)</term>
<term>RNA, Small Interfering (genetics)</term>
<term>Receptors, CXCR4 (genetics)</term>
<term>Signal Transduction (MeSH)</term>
<term>Vimentin (metabolism)</term>
<term>Xanthones (pharmacology)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr">
<term>Antigènes CD (génétique)</term>
<term>Antinéoplasiques d'origine végétale (pharmacologie)</term>
<term>Cadhérines (génétique)</term>
<term>Carcinome pulmonaire non à petites cellules (anatomopathologie)</term>
<term>Carcinome pulmonaire non à petites cellules (génétique)</term>
<term>Cellules A549 (MeSH)</term>
<term>Humains (MeSH)</term>
<term>Lignée cellulaire tumorale (MeSH)</term>
<term>Lipopolysaccharides (pharmacologie)</term>
<term>Mouvement cellulaire (effets des médicaments et des substances chimiques)</term>
<term>Mouvement cellulaire (génétique)</term>
<term>Petit ARN interférent (génétique)</term>
<term>Prolifération cellulaire (effets des médicaments et des substances chimiques)</term>
<term>Prolifération cellulaire (génétique)</term>
<term>Protéines circadiennes Period (génétique)</term>
<term>Récepteurs CXCR4 (génétique)</term>
<term>Régulation négative (MeSH)</term>
<term>Transduction du signal (MeSH)</term>
<term>Transition épithélio-mésenchymateuse (effets des médicaments et des substances chimiques)</term>
<term>Transition épithélio-mésenchymateuse (génétique)</term>
<term>Tumeurs du poumon (anatomopathologie)</term>
<term>Tumeurs du poumon (génétique)</term>
<term>Vimentine (métabolisme)</term>
<term>Xanthones (pharmacologie)</term>
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<term>Antigens, CD</term>
<term>Cadherins</term>
<term>Period Circadian Proteins</term>
<term>RNA, Small Interfering</term>
<term>Receptors, CXCR4</term>
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<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en">
<term>Vimentin</term>
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<term>Antineoplastic Agents, Phytogenic</term>
<term>Lipopolysaccharides</term>
<term>Xanthones</term>
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<keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr">
<term>Carcinome pulmonaire non à petites cellules</term>
<term>Tumeurs du poumon</term>
</keywords>
<keywords scheme="MESH" qualifier="drug effects" xml:lang="en">
<term>Cell Movement</term>
<term>Cell Proliferation</term>
<term>Epithelial-Mesenchymal Transition</term>
</keywords>
<keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr">
<term>Mouvement cellulaire</term>
<term>Prolifération cellulaire</term>
<term>Transition épithélio-mésenchymateuse</term>
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<keywords scheme="MESH" qualifier="genetics" xml:lang="en">
<term>Carcinoma, Non-Small-Cell Lung</term>
<term>Cell Movement</term>
<term>Cell Proliferation</term>
<term>Epithelial-Mesenchymal Transition</term>
<term>Lung Neoplasms</term>
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<keywords scheme="MESH" qualifier="génétique" xml:lang="fr">
<term>Antigènes CD</term>
<term>Cadhérines</term>
<term>Carcinome pulmonaire non à petites cellules</term>
<term>Mouvement cellulaire</term>
<term>Petit ARN interférent</term>
<term>Prolifération cellulaire</term>
<term>Protéines circadiennes Period</term>
<term>Récepteurs CXCR4</term>
<term>Transition épithélio-mésenchymateuse</term>
<term>Tumeurs du poumon</term>
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<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr">
<term>Vimentine</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en">
<term>Carcinoma, Non-Small-Cell Lung</term>
<term>Lung Neoplasms</term>
</keywords>
<keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr">
<term>Antinéoplasiques d'origine végétale</term>
<term>Lipopolysaccharides</term>
<term>Xanthones</term>
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<term>Cell Line, Tumor</term>
<term>Down-Regulation</term>
<term>Humans</term>
<term>Signal Transduction</term>
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<term>Humains</term>
<term>Lignée cellulaire tumorale</term>
<term>Régulation négative</term>
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<div type="abstract" xml:lang="en">Non-small cell lung cancer (NSCLC) is often complicated by pulmonary infection, which affects treatment and prognosis. Bacterial lipopolysaccharide (LPS) is an effective stimulator of inflammatory cytokine production, and previous studies have reported that LPS promotes tumor invasion and metastasis. Mangiferin is a plant-derived C-glucosylxanthone with many biological activities, such as antioxidation and anti-inflammation. This research mainly explored the mechanism of its antitumor activities on LPS-induced A549, NCI-H460, and NCI-H520 NSCLC cells. We determined that mangiferin exhibits growth inhibiting activity against LPS-induced NSCLC cells through the 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assay. In addition, mangiferin reversed the LPS-induced downregulation of E-cadherin (epithelial marker); conversely, it significantly inhibited the expression of raised vimentin (mesenchymal markers). Moreover, the ability of NSCLC cells to migrate, as evidenced by the wound healing and transwell migration assays, and the expression of CXCR4 increased by LPS were significantly repressed by mangiferin. In addition, mangiferin markedly mediated protein levels of PER1 and NLRP3 in LPS-induced NSCLC cells and reduced the secretion of IL-1β. These results indicate that mangiferin is not only a remarkable anti-inflammatory compound but also an antitumor agent; thus, it has the potential for being developed into anti-inflammatory and antitumor drugs in the future.</div>
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<Title>Environmental toxicology</Title>
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<ArticleTitle>Mangiferin inhibits lipopolysaccharide-induced epithelial-mesenchymal transition (EMT) and enhances the expression of tumor suppressor gene PER1 in non-small cell lung cancer cells.</ArticleTitle>
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<AbstractText>Non-small cell lung cancer (NSCLC) is often complicated by pulmonary infection, which affects treatment and prognosis. Bacterial lipopolysaccharide (LPS) is an effective stimulator of inflammatory cytokine production, and previous studies have reported that LPS promotes tumor invasion and metastasis. Mangiferin is a plant-derived C-glucosylxanthone with many biological activities, such as antioxidation and anti-inflammation. This research mainly explored the mechanism of its antitumor activities on LPS-induced A549, NCI-H460, and NCI-H520 NSCLC cells. We determined that mangiferin exhibits growth inhibiting activity against LPS-induced NSCLC cells through the 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assay. In addition, mangiferin reversed the LPS-induced downregulation of E-cadherin (epithelial marker); conversely, it significantly inhibited the expression of raised vimentin (mesenchymal markers). Moreover, the ability of NSCLC cells to migrate, as evidenced by the wound healing and transwell migration assays, and the expression of CXCR4 increased by LPS were significantly repressed by mangiferin. In addition, mangiferin markedly mediated protein levels of PER1 and NLRP3 in LPS-induced NSCLC cells and reduced the secretion of IL-1β. These results indicate that mangiferin is not only a remarkable anti-inflammatory compound but also an antitumor agent; thus, it has the potential for being developed into anti-inflammatory and antitumor drugs in the future.</AbstractText>
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<LastName>Lin</LastName>
<ForeName>Yen-Sung</ForeName>
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<Affiliation>Division of Pulmonary and Critical Care Medicine, An Nan Hospital, China Medical University, Tainan, Taiwan.</Affiliation>
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<LastName>Tsai</LastName>
<ForeName>Kun-Ling</ForeName>
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<Affiliation>Department of Physical Therapy, College of Medicine, National Cheng Kung University, Tainan, Taiwan.</Affiliation>
</AffiliationInfo>
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<ForeName>Jia-Ni</ForeName>
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<Affiliation>Department of Medical Sciences Industry, College of Health Sciences, Chang Jung Christian University, Tainan, Taiwan.</Affiliation>
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<LastName>Wu</LastName>
<ForeName>Chen-Shiou</ForeName>
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<AffiliationInfo>
<Affiliation>Department of Medical Sciences Industry, College of Health Sciences, Chang Jung Christian University, Tainan, Taiwan.</Affiliation>
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<Language>eng</Language>
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<GrantID>CJCU 108C120124</GrantID>
<Agency>Chang Jung Christian University, Tainan, Taiwan</Agency>
<Country></Country>
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<GrantID>MOST 107-2320-B-309-001</GrantID>
<Agency>Ministry of Science and Technology, Taiwan</Agency>
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<DescriptorName UI="D015703" MajorTopicYN="N">Antigens, CD</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
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<MeshHeading>
<DescriptorName UI="D000972" MajorTopicYN="N">Antineoplastic Agents, Phytogenic</DescriptorName>
<QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName>
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<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
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<DescriptorName UI="D002289" MajorTopicYN="N">Carcinoma, Non-Small-Cell Lung</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName>
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<MeshHeading>
<DescriptorName UI="D045744" MajorTopicYN="N">Cell Line, Tumor</DescriptorName>
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<DescriptorName UI="D002465" MajorTopicYN="N">Cell Movement</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D049109" MajorTopicYN="N">Cell Proliferation</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D015536" MajorTopicYN="N">Down-Regulation</DescriptorName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D058750" MajorTopicYN="N">Epithelial-Mesenchymal Transition</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
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<MeshHeading>
<DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName>
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<MeshHeading>
<DescriptorName UI="D008070" MajorTopicYN="N">Lipopolysaccharides</DescriptorName>
<QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName>
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<MeshHeading>
<DescriptorName UI="D008175" MajorTopicYN="N">Lung Neoplasms</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D056950" MajorTopicYN="N">Period Circadian Proteins</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
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<MeshHeading>
<DescriptorName UI="D034741" MajorTopicYN="N">RNA, Small Interfering</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
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<name sortKey="Chen, Jia Ni" sort="Chen, Jia Ni" uniqKey="Chen J" first="Jia-Ni" last="Chen">Jia-Ni Chen</name>
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