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 : 000118 ( PubMed/Corpus ); précédent : 000117; suivant : 000119Caffeic 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 ; Asami Tanimae ; Takumi Furuta ; Satoshi Endo ; Toshiyuki Matsunaga ; Kenji Ichihara ; Akira IkariSource :
- The Journal of nutritional biochemistry [ 1873-4847 ] ; 2018.
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
Links to Exploration step
pubmed:29597147Le document en format XML
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Electronic address: ikari@gifu-pu.ac.jp.</nlm:affiliation></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></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">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.</title><author><name sortKey="Sonoki, Hiroyuki" sort="Sonoki, Hiroyuki" uniqKey="Sonoki H" first="Hiroyuki" last="Sonoki">Hiroyuki Sonoki</name><affiliation><nlm:affiliation>Laboratory of Biochemistry, Department of Biopharmaceutical Sciences, Gifu Pharmaceutical University, Gifu 501-1196, Japan.</nlm:affiliation></affiliation></author><author><name sortKey="Tanimae, Asami" sort="Tanimae, Asami" uniqKey="Tanimae A" first="Asami" last="Tanimae">Asami Tanimae</name><affiliation><nlm:affiliation>Laboratory of Biochemistry, Department of Biopharmaceutical Sciences, Gifu Pharmaceutical University, Gifu 501-1196, Japan.</nlm:affiliation></affiliation></author><author><name sortKey="Furuta, Takumi" sort="Furuta, Takumi" uniqKey="Furuta T" first="Takumi" last="Furuta">Takumi Furuta</name><affiliation><nlm:affiliation>Institute for Chemical Research, Kyoto University, Kyoto 611-0011, Japan.</nlm:affiliation></affiliation></author><author><name sortKey="Endo, Satoshi" sort="Endo, Satoshi" uniqKey="Endo S" first="Satoshi" last="Endo">Satoshi Endo</name><affiliation><nlm:affiliation>Laboratory of Biochemistry, Department of Biopharmaceutical Sciences, Gifu Pharmaceutical University, Gifu 501-1196, Japan.</nlm:affiliation></affiliation></author><author><name sortKey="Matsunaga, Toshiyuki" sort="Matsunaga, Toshiyuki" uniqKey="Matsunaga T" first="Toshiyuki" last="Matsunaga">Toshiyuki Matsunaga</name><affiliation><nlm:affiliation>Laboratory of Biochemistry, Department of Biopharmaceutical Sciences, Gifu Pharmaceutical University, Gifu 501-1196, Japan.</nlm:affiliation></affiliation></author><author><name sortKey="Ichihara, Kenji" sort="Ichihara, Kenji" uniqKey="Ichihara K" first="Kenji" last="Ichihara">Kenji Ichihara</name><affiliation><nlm:affiliation>Nagaragawa Research Center, API Co., Ltd., Gifu 502-0071, Japan.</nlm:affiliation></affiliation></author><author><name sortKey="Ikari, Akira" sort="Ikari, Akira" uniqKey="Ikari A" first="Akira" last="Ikari">Akira Ikari</name><affiliation><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></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="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="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" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Doxorubicin</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></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><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">29597147</PMID><DateCompleted><Year>2019</Year><Month>09</Month><Day>04</Day></DateCompleted><DateRevised><Year>2019</Year><Month>09</Month><Day>04</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1873-4847</ISSN><JournalIssue CitedMedium="Internet"><Volume>56</Volume><PubDate><Year>2018</Year><Month>06</Month></PubDate></JournalIssue><Title>The Journal of nutritional biochemistry</Title><ISOAbbreviation>J. Nutr. Biochem.</ISOAbbreviation></Journal><ArticleTitle>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.</ArticleTitle><Pagination><MedlinePgn>205-214</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">S0955-2863(17)30782-9</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.jnutbio.2018.02.016</ELocationID><Abstract><AbstractText>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.</AbstractText><CopyrightInformation>Copyright © 2018 Elsevier Inc. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Sonoki</LastName><ForeName>Hiroyuki</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Laboratory of Biochemistry, Department of Biopharmaceutical Sciences, Gifu Pharmaceutical University, Gifu 501-1196, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tanimae</LastName><ForeName>Asami</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Laboratory of Biochemistry, Department of Biopharmaceutical Sciences, Gifu Pharmaceutical University, Gifu 501-1196, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Furuta</LastName><ForeName>Takumi</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Institute for Chemical Research, Kyoto University, Kyoto 611-0011, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Endo</LastName><ForeName>Satoshi</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Laboratory of Biochemistry, Department of Biopharmaceutical Sciences, Gifu Pharmaceutical University, Gifu 501-1196, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Matsunaga</LastName><ForeName>Toshiyuki</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Laboratory of Biochemistry, Department of Biopharmaceutical Sciences, Gifu Pharmaceutical University, Gifu 501-1196, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ichihara</LastName><ForeName>Kenji</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Nagaragawa Research Center, API Co., Ltd., Gifu 502-0071, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ikari</LastName><ForeName>Akira</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Laboratory of Biochemistry, Department of Biopharmaceutical Sciences, Gifu Pharmaceutical University, Gifu 501-1196, Japan. Electronic address: ikari@gifu-pu.ac.jp.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2018</Year><Month>03</Month><Day>02</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Nutr Biochem</MedlineTA><NlmUniqueID>9010081</NlmUniqueID><ISSNLinking>0955-2863</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C491875">CLDN2 protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D002109">Caffeic Acids</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D057167">Claudins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D005227">Fatty Acids</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D012333">RNA, Messenger</NameOfSubstance></Chemical><Chemical><RegistryNumber>80168379AG</RegistryNumber><NameOfSubstance UI="D004317">Doxorubicin</NameOfSubstance></Chemical><Chemical><RegistryNumber>886U3H6UFF</RegistryNumber><NameOfSubstance UI="D002738">Chloroquine</NameOfSubstance></Chemical><Chemical><RegistryNumber>9009-62-5</RegistryNumber><NameOfSubstance UI="D011429">Propolis</NameOfSubstance></Chemical><Chemical><RegistryNumber>G960R9S5SK</RegistryNumber><NameOfSubstance UI="C055494">caffeic acid phenethyl ester</NameOfSubstance></Chemical><Chemical><RegistryNumber>IGL471WQ8P</RegistryNumber><NameOfSubstance UI="D002193">Cantharidin</NameOfSubstance></Chemical><Chemical><RegistryNumber>L497I37F0C</RegistryNumber><NameOfSubstance UI="C058787">royal jelly</NameOfSubstance></Chemical><Chemical><RegistryNumber>ML9LGA7468</RegistryNumber><NameOfSubstance UI="D010626">Phenylethyl Alcohol</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000072283" MajorTopicYN="N">A549 Cells</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000077192" MajorTopicYN="N">Adenocarcinoma of Lung</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002109" MajorTopicYN="N">Caffeic Acids</DescriptorName><QualifierName UI="Q000737" MajorTopicYN="Y">chemistry</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002193" MajorTopicYN="N">Cantharidin</DescriptorName><QualifierName UI="Q000737" MajorTopicYN="N">chemistry</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="D002738" MajorTopicYN="N">Chloroquine</DescriptorName><QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D057167" MajorTopicYN="N">Claudins</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015536" MajorTopicYN="N">Down-Regulation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004317" MajorTopicYN="N">Doxorubicin</DescriptorName><QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004357" MajorTopicYN="N">Drug Synergism</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005227" MajorTopicYN="N">Fatty Acids</DescriptorName><QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005786" MajorTopicYN="Y">Gene Expression Regulation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008175" MajorTopicYN="N">Lung Neoplasms</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008247" MajorTopicYN="N">Lysosomes</DescriptorName><QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010539" MajorTopicYN="N">Permeability</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010626" MajorTopicYN="N">Phenylethyl Alcohol</DescriptorName><QualifierName UI="Q000031" MajorTopicYN="Y">analogs & derivatives</QualifierName><QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011401" MajorTopicYN="N">Promoter Regions, Genetic</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011429" MajorTopicYN="N">Propolis</DescriptorName><QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012333" MajorTopicYN="N">RNA, Messenger</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D019108" MajorTopicYN="N">Tight Junctions</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">3D culture</Keyword><Keyword MajorTopicYN="Y">CAPE</Keyword><Keyword MajorTopicYN="Y">Claudin-2</Keyword><Keyword MajorTopicYN="Y">Lung adenocarcinoma</Keyword><Keyword 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