Bruceine D induces lung cancer cell apoptosis and autophagy via the ROS/MAPK signaling pathway in vitro and in vivo
Identifieur interne : 000F38 ( Ncbi/Merge ); précédent : 000F37; suivant : 000F39Bruceine D induces lung cancer cell apoptosis and autophagy via the ROS/MAPK signaling pathway in vitro and in vivo
Auteurs : Jiangjiang Fan [République populaire de Chine] ; Dongmei Ren [République populaire de Chine] ; Jinxia Wang [République populaire de Chine] ; Xiaoqing Liu [République populaire de Chine] ; Huaran Zhang [République populaire de Chine] ; Mingsheng Wu [République populaire de Chine] ; Guotao Yang [République populaire de Chine]Source :
- Cell Death & Disease [ 2041-4889 ] ; 2020.
Abstract
Worldwide, lung cancer remains a leading cause of cancer mortality. Bruceine D (BD) has been shown to induce pancreatic cancer cell death via several different mechanisms. In this study, we demonstrated that BD inhibited lung cancer cell proliferation. Apoptosis and autophagy were the most important mechanisms involved in BD-induced lung cancer cell death, and complete autophagic flux was observed in A549 and NCI-H292 cells. In addition, BD significantly improved intracellular reactive oxygen species (ROS) levels. BD-mediated cell apoptosis and autophagy were almost inhibited in cells pretreated with N-acetylcysteine (NAC), an ROS scavenger. Furthermore, MAPK signaling pathway activation contributed to BD-induced cell proliferation inhibition and NAC could eliminate p-ERK and p-JNK upregulation. Finally, an in vivo study indicated that BD inhibited the growth of lung cancer xenografts. Overall, BD is a promising candidate for the treatment of lung cancer owing to its multiple mechanisms and low toxicity.
Url:
DOI: 10.1038/s41419-020-2317-3
PubMed: 32071301
PubMed Central: 7028916
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China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>107 West Wenhua Road, Jinan</wicri:regionArea><wicri:noRegion>Jinan</wicri:noRegion></affiliation></author><author><name sortKey="Yang, Guotao" sort="Yang, Guotao" uniqKey="Yang G" first="Guotao" last="Yang">Guotao Yang</name><affiliation wicri:level="1"><nlm:aff id="Aff1"><institution-wrap><institution-id institution-id-type="GRID">grid.452402.5</institution-id><institution>Department of Thoracic Surgery,</institution><institution>Qilu Hospital of Shandong University,</institution></institution-wrap>107 West Wenhua Road, Jinan, 250012 P. R. China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>107 West Wenhua Road, Jinan</wicri:regionArea><wicri:noRegion>Jinan</wicri:noRegion></affiliation></author></analytic><series><title level="j">Cell Death & Disease</title><idno type="eISSN">2041-4889</idno><imprint><date when="2020">2020</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p id="Par1">Worldwide, lung cancer remains a leading cause of cancer mortality. Bruceine D (BD) has been shown to induce pancreatic cancer cell death via several different mechanisms. In this study, we demonstrated that BD inhibited lung cancer cell proliferation. Apoptosis and autophagy were the most important mechanisms involved in BD-induced lung cancer cell death, and complete autophagic flux was observed in A549 and NCI-H292 cells. In addition, BD significantly improved intracellular reactive oxygen species (ROS) levels. BD-mediated cell apoptosis and autophagy were almost inhibited in cells pretreated with N-acetylcysteine (NAC), an ROS scavenger. Furthermore, MAPK signaling pathway activation contributed to BD-induced cell proliferation inhibition and NAC could eliminate p-ERK and p-JNK upregulation. Finally, an in vivo study indicated that BD inhibited the growth of lung cancer xenografts. Overall, BD is a promising candidate for the treatment of lung cancer owing to its multiple mechanisms and low toxicity.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Siegel, Rl" uniqKey="Siegel R">RL Siegel</name></author><author><name sortKey="Miller, Kd" uniqKey="Miller K">KD Miller</name></author><author><name sortKey="Jemal, A" uniqKey="Jemal A">A Jemal</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Valastyan, S" uniqKey="Valastyan S">S Valastyan</name></author><author><name sortKey="Weinberg, Ra" uniqKey="Weinberg R">RA Weinberg</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Groome, Pa" uniqKey="Groome P">PA Groome</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Subeki" uniqKey="Subeki">Subeki.</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Zhao, L" uniqKey="Zhao L">L 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<front><journal-meta><journal-id journal-id-type="nlm-ta">Cell Death Dis</journal-id><journal-id journal-id-type="iso-abbrev">Cell Death Dis</journal-id><journal-title-group><journal-title>Cell Death & Disease</journal-title></journal-title-group><issn pub-type="epub">2041-4889</issn><publisher><publisher-name>Nature Publishing Group UK</publisher-name><publisher-loc>London</publisher-loc></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">32071301</article-id><article-id pub-id-type="pmc">7028916</article-id><article-id pub-id-type="publisher-id">2317</article-id><article-id pub-id-type="doi">10.1038/s41419-020-2317-3</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title-group><article-title>Bruceine D induces lung cancer cell apoptosis and autophagy via the ROS/MAPK signaling pathway in vitro and in vivo</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Fan</surname><given-names>Jiangjiang</given-names></name><xref ref-type="aff" rid="Aff1">1</xref></contrib><contrib contrib-type="author"><name><surname>Ren</surname><given-names>Dongmei</given-names></name><xref ref-type="aff" rid="Aff2">2</xref></contrib><contrib contrib-type="author"><name><surname>Wang</surname><given-names>Jinxia</given-names></name><xref ref-type="aff" rid="Aff2">2</xref></contrib><contrib contrib-type="author"><name><surname>Liu</surname><given-names>Xiaoqing</given-names></name><xref ref-type="aff" rid="Aff2">2</xref></contrib><contrib contrib-type="author"><name><surname>Zhang</surname><given-names>Huaran</given-names></name><xref ref-type="aff" rid="Aff2">2</xref></contrib><contrib contrib-type="author"><name><surname>Wu</surname><given-names>Mingsheng</given-names></name><xref ref-type="aff" rid="Aff1">1</xref></contrib><contrib contrib-type="author" corresp="yes"><name><surname>Yang</surname><given-names>Guotao</given-names></name><address><email>yanggtxwk@163.com</email></address><xref ref-type="aff" rid="Aff1">1</xref></contrib><aff id="Aff1"><label>1</label><institution-wrap><institution-id institution-id-type="GRID">grid.452402.5</institution-id><institution>Department of Thoracic Surgery,</institution><institution>Qilu Hospital of Shandong University,</institution></institution-wrap>107 West Wenhua Road, Jinan, 250012 P. R. China</aff><aff id="Aff2"><label>2</label><institution-wrap><institution-id institution-id-type="ISNI">0000 0004 1761 1174</institution-id><institution-id institution-id-type="GRID">grid.27255.37</institution-id><institution>Key Laboratory of Chemical Biology (Ministry of Education), School of Pharmaceutical Sciences, Shandong University,</institution></institution-wrap>44 West Wenhua Road, Jinan, 250012 P. R. China</aff></contrib-group><pub-date pub-type="epub"><day>18</day><month>2</month><year>2020</year></pub-date><pub-date pub-type="pmc-release"><day>18</day><month>2</month><year>2020</year></pub-date><pub-date pub-type="collection"><month>2</month><year>2020</year></pub-date><volume>11</volume><issue>2</issue><elocation-id>126</elocation-id><history><date date-type="received"><day>14</day><month>10</month><year>2019</year></date><date date-type="rev-recd"><day>30</day><month>1</month><year>2020</year></date><date date-type="accepted"><day>31</day><month>1</month><year>2020</year></date></history><permissions><copyright-statement>© The Author(s) 2020</copyright-statement><license license-type="OpenAccess"><license-p><bold>Open Access</bold> This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit <ext-link ext-link-type="uri" xlink:href="http://creativecommons.org/licenses/by/4.0/">http://creativecommons.org/licenses/by/4.0/</ext-link>.</license-p></license></permissions><abstract id="Abs1"><p id="Par1">Worldwide, lung cancer remains a leading cause of cancer mortality. Bruceine D (BD) has been shown to induce pancreatic cancer cell death via several different mechanisms. In this study, we demonstrated that BD inhibited lung cancer cell proliferation. Apoptosis and autophagy were the most important mechanisms involved in BD-induced lung cancer cell death, and complete autophagic flux was observed in A549 and NCI-H292 cells. In addition, BD significantly improved intracellular reactive oxygen species (ROS) levels. BD-mediated cell apoptosis and autophagy were almost inhibited in cells pretreated with N-acetylcysteine (NAC), an ROS scavenger. Furthermore, MAPK signaling pathway activation contributed to BD-induced cell proliferation inhibition and NAC could eliminate p-ERK and p-JNK upregulation. Finally, an in vivo study indicated that BD inhibited the growth of lung cancer xenografts. Overall, BD is a promising candidate for the treatment of lung cancer owing to its multiple mechanisms and low toxicity.</p></abstract><kwd-group kwd-group-type="npg-subject"><title>Subject terms</title><kwd>Non-small-cell lung cancer</kwd><kwd>Autophagy</kwd><kwd>Toxicology</kwd></kwd-group><custom-meta-group><custom-meta><meta-name>issue-copyright-statement</meta-name><meta-value>© The Author(s) 2020</meta-value></custom-meta></custom-meta-group></article-meta></front></pmc><affiliations><list><country><li>République populaire de Chine</li></country></list><tree><country name="République populaire de Chine"><noRegion><name sortKey="Fan, Jiangjiang" sort="Fan, Jiangjiang" uniqKey="Fan J" first="Jiangjiang" last="Fan">Jiangjiang Fan</name></noRegion><name sortKey="Liu, Xiaoqing" sort="Liu, Xiaoqing" uniqKey="Liu X" first="Xiaoqing" last="Liu">Xiaoqing Liu</name><name sortKey="Ren, Dongmei" sort="Ren, Dongmei" uniqKey="Ren D" first="Dongmei" last="Ren">Dongmei Ren</name><name sortKey="Wang, Jinxia" sort="Wang, Jinxia" uniqKey="Wang J" first="Jinxia" last="Wang">Jinxia Wang</name><name sortKey="Wu, Mingsheng" sort="Wu, Mingsheng" uniqKey="Wu M" first="Mingsheng" last="Wu">Mingsheng Wu</name><name sortKey="Yang, Guotao" sort="Yang, Guotao" uniqKey="Yang G" first="Guotao" last="Yang">Guotao Yang</name><name sortKey="Zhang, Huaran" sort="Zhang, Huaran" uniqKey="Zhang H" first="Huaran" last="Zhang">Huaran Zhang</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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