Caffeic acid phenethyl ester down-regulates claudin-2 expression at the transcriptional and post-translational levels and enhances chemosensitivity to doxorubicin in lung adenocarcinoma A549 cells.
Identifieur interne : 000C46 ( Main/Exploration ); précédent : 000C45; suivant : 000C47Caffeic acid phenethyl ester down-regulates claudin-2 expression at the transcriptional and post-translational levels and enhances chemosensitivity to doxorubicin in lung adenocarcinoma A549 cells.
Auteurs : Hiroyuki Sonoki [Japon] ; Asami Tanimae [Japon] ; Takumi Furuta [Japon] ; Satoshi Endo [Japon] ; Toshiyuki Matsunaga [Japon] ; Kenji Ichihara [Japon] ; Akira Ikari [Japon]Source :
- The Journal of nutritional biochemistry [ 1873-4847 ] ; 2018.
Descripteurs français
- KwdFr :
- ARN messager (métabolisme), Acides caféiques (), Acides gras (), Alcool phénéthylique (), Alcool phénéthylique (analogues et dérivés), Cantharidine (), Cellules A549, Chloroquine (), Claudines (métabolisme), Doxorubicine (), Doxorubicine (pharmacologie), Humains, Jonctions serrées, Lignée cellulaire tumorale, Lysosomes (), Perméabilité, Prolifération cellulaire, Propolis (), Régions promotrices (génétique), Régulation de l'expression des gènes, Régulation négative, Synergie des médicaments, Tumeurs du poumon (métabolisme), Tumeurs du poumon (traitement médicamenteux).
- MESH :
- analogues et dérivés : Alcool phénéthylique.
- métabolisme : ARN messager, Claudines, Tumeurs du poumon.
- pharmacologie : Doxorubicine.
- traitement médicamenteux : Tumeurs du poumon.
- Acides caféiques, Acides gras, Alcool phénéthylique, Cantharidine, Cellules A549, Chloroquine, Doxorubicine, Humains, Jonctions serrées, Lignée cellulaire tumorale, Lysosomes, Perméabilité, Prolifération cellulaire, Propolis, Régions promotrices (génétique), Régulation de l'expression des gènes, Régulation négative, Synergie des médicaments.
English descriptors
- KwdEn :
- A549 Cells, Adenocarcinoma of Lung (drug therapy), Adenocarcinoma of Lung (metabolism), Caffeic Acids (chemistry), Cantharidin (chemistry), Cell Line, Tumor, Cell Proliferation, Chloroquine (chemistry), Claudins (metabolism), Down-Regulation, Doxorubicin (chemistry), Doxorubicin (pharmacology), Drug Synergism, Fatty Acids (chemistry), Gene Expression Regulation, Humans, Lung Neoplasms (drug therapy), Lung Neoplasms (metabolism), Lysosomes (chemistry), Permeability, Phenylethyl Alcohol (analogs & derivatives), Phenylethyl Alcohol (chemistry), Promoter Regions, Genetic, Propolis (chemistry), RNA, Messenger (metabolism), Tight Junctions.
- MESH :
- chemical , analogs & derivatives : Phenylethyl Alcohol.
- chemical , chemistry : Caffeic Acids, Cantharidin, Chloroquine, Doxorubicin, Fatty Acids, Phenylethyl Alcohol, Propolis.
- chemistry : Lysosomes.
- drug therapy : Adenocarcinoma of Lung, Lung Neoplasms.
- metabolism : Adenocarcinoma of Lung, Claudins, Lung Neoplasms, RNA, Messenger.
- chemical , pharmacology : Doxorubicin.
- A549 Cells, Cell Line, Tumor, Cell Proliferation, Down-Regulation, Drug Synergism, Gene Expression Regulation, Humans, Permeability, Promoter Regions, Genetic, Tight Junctions.
Abstract
Claudin-2 is highly expressed in human lung adenocarcinoma cells and involved in the promotion of proliferation. Here, we searched for a compound, which can decrease claudin-2 expression using lung adenocarcinoma A549 cells. In the screening using compounds included in royal jelly and propolis, the protein level of claudin-2 was dose-dependently decreased by caffeic acid phenethyl ester (CAPE), whereas the mRNA level and promoter activity were only decreased by 50 μM CAPE. These results suggest that CAPE down-regulates claudin-2 expression mediated by two different mechanisms. CAPE (50 μM) decreased the level of p-NF-κB, whereas it increased that of IκB. The CAPE-induced decrease in promoter activity of claudin-2 was blocked by the mutation in an NF-κB-binding site. The inhibition of NF-κB may be involved in the decrease in mRNA level of claudin-2. The CAPE (10 μM)-induced decrease in claudin-2 expression was inhibited by chloroquine, a lysosomal inhibitor. CAPE increased the expression and activity of protein phosphatase (PP) 1 and 2A. The CAPE-induced decrease in claudin-2 expression was blocked by cantharidin, a potent PPs inhibitor. The cell proliferation was suppressed by CAPE, which was partially rescued by ectopic expression of claudin-2. In addition, the toxicity and accumulation of doxorubicin in 3D spheroid cells were enhanced by CAPE, which was inhibited by ectopic expression of claudin-2. Taken together, CAPE down-regulates claudin-2 expression at the transcriptional and post-translational levels, and enhances sensitivity of cells to doxorubicin in 3D culture conditions. CAPE may be a useful adjunctive compound in the treatment of lung adenocarcinoma.
DOI: 10.1016/j.jnutbio.2018.02.016
PubMed: 29597147
Affiliations:
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Le document en format XML
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Electronic address: ikari@gifu-pu.ac.jp.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Laboratory of Biochemistry, Department of Biopharmaceutical Sciences, Gifu Pharmaceutical University, Gifu 501-1196</wicri:regionArea><wicri:noRegion>Gifu 501-1196</wicri:noRegion></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2018">2018</date><idno type="RBID">pubmed:29597147</idno><idno type="pmid">29597147</idno><idno type="doi">10.1016/j.jnutbio.2018.02.016</idno><idno type="wicri:Area/PubMed/Corpus">000118</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000118</idno><idno type="wicri:Area/PubMed/Curation">000118</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">000118</idno><idno type="wicri:Area/PubMed/Checkpoint">000119</idno><idno type="wicri:explorRef" wicri:stream="Checkpoint" wicri:step="PubMed">000119</idno><idno 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Biopharmaceutical Sciences, Gifu Pharmaceutical University, Gifu 501-1196</wicri:regionArea><wicri:noRegion>Gifu 501-1196</wicri:noRegion></affiliation></author><author><name sortKey="Tanimae, Asami" sort="Tanimae, Asami" uniqKey="Tanimae A" first="Asami" last="Tanimae">Asami Tanimae</name><affiliation wicri:level="1"><nlm:affiliation>Laboratory of Biochemistry, Department of Biopharmaceutical Sciences, Gifu Pharmaceutical University, Gifu 501-1196, Japan.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Laboratory of Biochemistry, Department of Biopharmaceutical Sciences, Gifu Pharmaceutical University, Gifu 501-1196</wicri:regionArea><wicri:noRegion>Gifu 501-1196</wicri:noRegion></affiliation></author><author><name sortKey="Furuta, Takumi" sort="Furuta, Takumi" uniqKey="Furuta T" first="Takumi" last="Furuta">Takumi Furuta</name><affiliation wicri:level="4"><nlm:affiliation>Institute for Chemical Research, Kyoto University, Kyoto 611-0011, Japan.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Institute for Chemical Research, Kyoto University, Kyoto 611-0011</wicri:regionArea><orgName type="university">Université de Kyoto</orgName><placeName><settlement type="city">Kyoto</settlement><region type="prefecture">Région du Kansai</region></placeName></affiliation></author><author><name sortKey="Endo, Satoshi" sort="Endo, Satoshi" uniqKey="Endo S" first="Satoshi" last="Endo">Satoshi Endo</name><affiliation wicri:level="1"><nlm:affiliation>Laboratory of Biochemistry, Department of Biopharmaceutical Sciences, Gifu Pharmaceutical University, Gifu 501-1196, Japan.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Laboratory of Biochemistry, Department of Biopharmaceutical Sciences, Gifu Pharmaceutical University, Gifu 501-1196</wicri:regionArea><wicri:noRegion>Gifu 501-1196</wicri:noRegion></affiliation></author><author><name sortKey="Matsunaga, Toshiyuki" sort="Matsunaga, Toshiyuki" uniqKey="Matsunaga T" first="Toshiyuki" last="Matsunaga">Toshiyuki Matsunaga</name><affiliation wicri:level="1"><nlm:affiliation>Laboratory of Biochemistry, Department of Biopharmaceutical Sciences, Gifu Pharmaceutical University, Gifu 501-1196, Japan.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Laboratory of Biochemistry, Department of Biopharmaceutical Sciences, Gifu Pharmaceutical University, Gifu 501-1196</wicri:regionArea><wicri:noRegion>Gifu 501-1196</wicri:noRegion></affiliation></author><author><name sortKey="Ichihara, Kenji" sort="Ichihara, Kenji" uniqKey="Ichihara K" first="Kenji" last="Ichihara">Kenji Ichihara</name><affiliation wicri:level="1"><nlm:affiliation>Nagaragawa Research Center, API Co., Ltd., Gifu 502-0071, Japan.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Nagaragawa Research Center, API Co., Ltd., Gifu 502-0071</wicri:regionArea><wicri:noRegion>Gifu 502-0071</wicri:noRegion></affiliation></author><author><name sortKey="Ikari, Akira" sort="Ikari, Akira" uniqKey="Ikari A" first="Akira" last="Ikari">Akira Ikari</name><affiliation wicri:level="1"><nlm:affiliation>Laboratory of Biochemistry, Department of Biopharmaceutical Sciences, Gifu Pharmaceutical University, Gifu 501-1196, Japan. Electronic address: ikari@gifu-pu.ac.jp.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Laboratory of Biochemistry, Department of Biopharmaceutical Sciences, Gifu Pharmaceutical University, Gifu 501-1196</wicri:regionArea><wicri:noRegion>Gifu 501-1196</wicri:noRegion></affiliation></author></analytic><series><title level="j">The Journal of nutritional biochemistry</title><idno type="eISSN">1873-4847</idno><imprint><date when="2018" type="published">2018</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>A549 Cells</term><term>Adenocarcinoma of Lung (drug therapy)</term><term>Adenocarcinoma of Lung (metabolism)</term><term>Caffeic Acids (chemistry)</term><term>Cantharidin (chemistry)</term><term>Cell Line, Tumor</term><term>Cell Proliferation</term><term>Chloroquine (chemistry)</term><term>Claudins (metabolism)</term><term>Down-Regulation</term><term>Doxorubicin (chemistry)</term><term>Doxorubicin (pharmacology)</term><term>Drug Synergism</term><term>Fatty Acids (chemistry)</term><term>Gene Expression Regulation</term><term>Humans</term><term>Lung Neoplasms (drug therapy)</term><term>Lung Neoplasms (metabolism)</term><term>Lysosomes (chemistry)</term><term>Permeability</term><term>Phenylethyl Alcohol (analogs & derivatives)</term><term>Phenylethyl Alcohol (chemistry)</term><term>Promoter Regions, Genetic</term><term>Propolis (chemistry)</term><term>RNA, Messenger (metabolism)</term><term>Tight Junctions</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>ARN messager (métabolisme)</term><term>Acides caféiques ()</term><term>Acides gras ()</term><term>Alcool phénéthylique ()</term><term>Alcool phénéthylique (analogues et dérivés)</term><term>Cantharidine ()</term><term>Cellules A549</term><term>Chloroquine ()</term><term>Claudines (métabolisme)</term><term>Doxorubicine ()</term><term>Doxorubicine (pharmacologie)</term><term>Humains</term><term>Jonctions serrées</term><term>Lignée cellulaire tumorale</term><term>Lysosomes ()</term><term>Perméabilité</term><term>Prolifération cellulaire</term><term>Propolis ()</term><term>Régions promotrices (génétique)</term><term>Régulation de l'expression des gènes</term><term>Régulation négative</term><term>Synergie des médicaments</term><term>Tumeurs du poumon (métabolisme)</term><term>Tumeurs du poumon (traitement médicamenteux)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analogs & derivatives" xml:lang="en"><term>Phenylethyl Alcohol</term></keywords><keywords scheme="MESH" type="chemical" qualifier="chemistry" xml:lang="en"><term>Caffeic Acids</term><term>Cantharidin</term><term>Chloroquine</term><term>Doxorubicin</term><term>Fatty Acids</term><term>Phenylethyl Alcohol</term><term>Propolis</term></keywords><keywords scheme="MESH" qualifier="analogues et dérivés" xml:lang="fr"><term>Alcool phénéthylique</term></keywords><keywords scheme="MESH" qualifier="chemistry" xml:lang="en"><term>Lysosomes</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Adenocarcinoma of Lung</term><term>Lung Neoplasms</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Adenocarcinoma of Lung</term><term>Claudins</term><term>Lung Neoplasms</term><term>RNA, Messenger</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>ARN messager</term><term>Claudines</term><term>Tumeurs du poumon</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Doxorubicine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Doxorubicin</term></keywords><keywords scheme="MESH" qualifier="traitement médicamenteux" xml:lang="fr"><term>Tumeurs du poumon</term></keywords><keywords scheme="MESH" xml:lang="en"><term>A549 Cells</term><term>Cell Line, Tumor</term><term>Cell Proliferation</term><term>Down-Regulation</term><term>Drug Synergism</term><term>Gene Expression Regulation</term><term>Humans</term><term>Permeability</term><term>Promoter Regions, Genetic</term><term>Tight Junctions</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Acides caféiques</term><term>Acides gras</term><term>Alcool phénéthylique</term><term>Cantharidine</term><term>Cellules A549</term><term>Chloroquine</term><term>Doxorubicine</term><term>Humains</term><term>Jonctions serrées</term><term>Lignée cellulaire tumorale</term><term>Lysosomes</term><term>Perméabilité</term><term>Prolifération cellulaire</term><term>Propolis</term><term>Régions promotrices (génétique)</term><term>Régulation de l'expression des gènes</term><term>Régulation négative</term><term>Synergie des médicaments</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Claudin-2 is highly expressed in human lung adenocarcinoma cells and involved in the promotion of proliferation. Here, we searched for a compound, which can decrease claudin-2 expression using lung adenocarcinoma A549 cells. In the screening using compounds included in royal jelly and propolis, the protein level of claudin-2 was dose-dependently decreased by caffeic acid phenethyl ester (CAPE), whereas the mRNA level and promoter activity were only decreased by 50 μM CAPE. These results suggest that CAPE down-regulates claudin-2 expression mediated by two different mechanisms. CAPE (50 μM) decreased the level of p-NF-κB, whereas it increased that of IκB. The CAPE-induced decrease in promoter activity of claudin-2 was blocked by the mutation in an NF-κB-binding site. The inhibition of NF-κB may be involved in the decrease in mRNA level of claudin-2. The CAPE (10 μM)-induced decrease in claudin-2 expression was inhibited by chloroquine, a lysosomal inhibitor. CAPE increased the expression and activity of protein phosphatase (PP) 1 and 2A. The CAPE-induced decrease in claudin-2 expression was blocked by cantharidin, a potent PPs inhibitor. The cell proliferation was suppressed by CAPE, which was partially rescued by ectopic expression of claudin-2. In addition, the toxicity and accumulation of doxorubicin in 3D spheroid cells were enhanced by CAPE, which was inhibited by ectopic expression of claudin-2. Taken together, CAPE down-regulates claudin-2 expression at the transcriptional and post-translational levels, and enhances sensitivity of cells to doxorubicin in 3D culture conditions. CAPE may be a useful adjunctive compound in the treatment of lung adenocarcinoma.</div></front></TEI><affiliations><list><country><li>Japon</li></country><region><li>Région du Kansai</li></region><settlement><li>Kyoto</li></settlement><orgName><li>Université de Kyoto</li></orgName></list><tree><country name="Japon"><noRegion><name sortKey="Sonoki, Hiroyuki" sort="Sonoki, Hiroyuki" uniqKey="Sonoki H" first="Hiroyuki" last="Sonoki">Hiroyuki Sonoki</name></noRegion><name sortKey="Endo, Satoshi" sort="Endo, Satoshi" uniqKey="Endo S" first="Satoshi" last="Endo">Satoshi Endo</name><name sortKey="Furuta, Takumi" sort="Furuta, Takumi" uniqKey="Furuta T" first="Takumi" last="Furuta">Takumi Furuta</name><name sortKey="Ichihara, Kenji" sort="Ichihara, Kenji" uniqKey="Ichihara K" first="Kenji" last="Ichihara">Kenji Ichihara</name><name sortKey="Ikari, Akira" sort="Ikari, Akira" uniqKey="Ikari A" first="Akira" last="Ikari">Akira Ikari</name><name sortKey="Matsunaga, Toshiyuki" sort="Matsunaga, Toshiyuki" uniqKey="Matsunaga T" first="Toshiyuki" last="Matsunaga">Toshiyuki Matsunaga</name><name sortKey="Tanimae, Asami" sort="Tanimae, Asami" uniqKey="Tanimae A" first="Asami" last="Tanimae">Asami Tanimae</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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