Avenanthramide A triggers potent ROS-mediated anti-tumor effects in colorectal cancer by directly targeting DDX3
Identifieur interne : 000066 ( Pmc/Curation ); précédent : 000065; suivant : 000067Avenanthramide A triggers potent ROS-mediated anti-tumor effects in colorectal cancer by directly targeting DDX3
Auteurs : Rong Fu [République populaire de Chine] ; Peng Yang [République populaire de Chine] ; Zongwei Li [États-Unis] ; Wen Liu [République populaire de Chine] ; Sajid Amin [République populaire de Chine] ; Zhuoyu Li [République populaire de Chine]Source :
- Cell Death & Disease [ 2041-4889 ] ; 2019.
Abstract
Colorectal cancer (CRC) is a common malignant gastrointestinal tumor with high mortality worldwide. Drug resistance and cytotoxicity to normal cells are the main causes of chemotherapeutic treatment failure in CRC. Therefore, extracting the bioactive compounds from natural products with anti-carcinogenic activity and minimal side-effects is a promising strategy against CRC. The present study aims to evaluate the anti-carcinogenic properties of avenanthramides (AVNs) extracted from oats bran and clarify the underlying molecular mechanisms. We demonstrated that AVNs treatment suppressed mitochondrial bioenergetic generation, resulting in mitochondrial swelling and increased reactive oxygen species (ROS) production. Further study indicated that AVNs treatment significantly reduced DDX3 expression, an oncogenic RNA helicase highly expressed in human CRC tissues. DDX3 overexpression reversed the ROS-mediated CRC apoptosis induced by AVNs. Of note, we identified Avenanthramide A (AVN A) as the effective ingredient in AVNs extracts. AVN A blocked the ATPase activity of DDX3 and induced its degradation by directly binding to the Arg287 and Arg294 residues in DDX3. In conclusion, these innovative findings highlight that AVNs extracts, in particular its bioactive compound AVN A may crack the current hurdles in the way of CRC treatment.
Url:
DOI: 10.1038/s41419-019-1825-5
PubMed: 31391454
PubMed Central: 6685981
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type="abstract" xml:lang="en"><p id="Par1">Colorectal cancer (CRC) is a common malignant gastrointestinal tumor with high mortality worldwide. Drug resistance and cytotoxicity to normal cells are the main causes of chemotherapeutic treatment failure in CRC. Therefore, extracting the bioactive compounds from natural products with anti-carcinogenic activity and minimal side-effects is a promising strategy against CRC. The present study aims to evaluate the anti-carcinogenic properties of avenanthramides (AVNs) extracted from oats bran and clarify the underlying molecular mechanisms. We demonstrated that AVNs treatment suppressed mitochondrial bioenergetic generation, resulting in mitochondrial swelling and increased reactive oxygen species (ROS) production. Further study indicated that AVNs treatment significantly reduced DDX3 expression, an oncogenic RNA helicase highly expressed in human CRC tissues. DDX3 overexpression reversed the ROS-mediated CRC apoptosis induced by AVNs. Of note, we identified Avenanthramide A (AVN A) as the effective ingredient in AVNs extracts. AVN A blocked the ATPase activity of DDX3 and induced its degradation by directly binding to the Arg287 and Arg294 residues in DDX3. In conclusion, these innovative findings highlight that AVNs extracts, in particular its bioactive compound AVN A may crack the current hurdles in the way of CRC treatment.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Brenner, H" uniqKey="Brenner H">H Brenner</name></author><author><name sortKey="Kloor, M" uniqKey="Kloor M">M Kloor</name></author><author><name sortKey="Pox, Cp" uniqKey="Pox C">CP Pox</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Shanmugam, Mk" uniqKey="Shanmugam M">MK Shanmugam</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Yu, X" uniqKey="Yu X">X Yu</name></author><author><name sortKey="Yang, M" uniqKey="Yang M">M Yang</name></author><author><name sortKey="Dong, J" uniqKey="Dong J">J Dong</name></author><author><name sortKey="Shen, R" uniqKey="Shen R">R Shen</name></author></analytic></biblStruct><biblStruct><analytic><author><name 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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">31391454</article-id><article-id pub-id-type="pmc">6685981</article-id><article-id pub-id-type="publisher-id">1825</article-id><article-id pub-id-type="doi">10.1038/s41419-019-1825-5</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title-group><article-title>Avenanthramide A triggers potent ROS-mediated anti-tumor effects in colorectal cancer by directly targeting DDX3</article-title></title-group><contrib-group><contrib contrib-type="author" equal-contrib="yes"><name><surname>Fu</surname><given-names>Rong</given-names></name><xref ref-type="aff" rid="Aff1">1</xref><xref ref-type="aff" rid="Aff2">2</xref></contrib><contrib contrib-type="author" equal-contrib="yes"><name><surname>Yang</surname><given-names>Peng</given-names></name><xref ref-type="aff" rid="Aff1">1</xref><xref ref-type="aff" rid="Aff2">2</xref></contrib><contrib contrib-type="author"><name><surname>Li</surname><given-names>Zongwei</given-names></name><xref ref-type="aff" rid="Aff3">3</xref></contrib><contrib contrib-type="author"><name><surname>Liu</surname><given-names>Wen</given-names></name><xref ref-type="aff" rid="Aff1">1</xref></contrib><contrib contrib-type="author"><name><surname>Amin</surname><given-names>Sajid</given-names></name><xref ref-type="aff" rid="Aff1">1</xref></contrib><contrib contrib-type="author" corresp="yes"><name><surname>Li</surname><given-names>Zhuoyu</given-names></name><address><email>lzy@sxu.edu.cn</email></address><xref ref-type="aff" rid="Aff1">1</xref><xref ref-type="aff" rid="Aff4">4</xref></contrib><aff id="Aff1"><label>1</label><institution-wrap><institution-id institution-id-type="ISNI">0000 0004 1760 2008</institution-id><institution-id institution-id-type="GRID">grid.163032.5</institution-id><institution>Institute of Biotechnology, Key Laboratory of Chemical Biology and Molecular Engineering of National Ministry of Education,</institution><institution>Shanxi University,</institution></institution-wrap>Taiyuan, 030006 China</aff><aff id="Aff2"><label>2</label><institution-wrap><institution-id institution-id-type="ISNI">0000 0004 1760 2008</institution-id><institution-id institution-id-type="GRID">grid.163032.5</institution-id><institution>Institutes of Biomedical Sciences,</institution><institution>Shanxi University,</institution></institution-wrap>Taiyuan, 030006 China</aff><aff id="Aff3"><label>3</label><institution-wrap><institution-id institution-id-type="ISNI">0000 0001 2291 4776</institution-id><institution-id institution-id-type="GRID">grid.240145.6</institution-id><institution>Department of Lymphoma and Myeloma, Center for Cancer Immunology Research,</institution><institution>The University of Texas MD Anderson Cancer Center,</institution></institution-wrap>Houston, Texas 77030 USA</aff><aff id="Aff4"><label>4</label><institution-wrap><institution-id institution-id-type="ISNI">0000 0004 1760 2008</institution-id><institution-id institution-id-type="GRID">grid.163032.5</institution-id><institution>School of Life Science,</institution><institution>Shanxi University,</institution></institution-wrap>Taiyuan, 030006 China</aff></contrib-group><pub-date pub-type="epub"><day>7</day><month>8</month><year>2019</year></pub-date><pub-date pub-type="pmc-release"><day>7</day><month>8</month><year>2019</year></pub-date><pub-date pub-type="collection"><month>8</month><year>2019</year></pub-date><volume>10</volume><issue>8</issue><elocation-id>593</elocation-id><history><date date-type="received"><day>12</day><month>2</month><year>2019</year></date><date date-type="rev-recd"><day>11</day><month>7</month><year>2019</year></date><date date-type="accepted"><day>15</day><month>7</month><year>2019</year></date></history><permissions><copyright-statement>© The Author(s) 2019</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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, 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">Colorectal cancer (CRC) is a common malignant gastrointestinal tumor with high mortality worldwide. Drug resistance and cytotoxicity to normal cells are the main causes of chemotherapeutic treatment failure in CRC. Therefore, extracting the bioactive compounds from natural products with anti-carcinogenic activity and minimal side-effects is a promising strategy against CRC. The present study aims to evaluate the anti-carcinogenic properties of avenanthramides (AVNs) extracted from oats bran and clarify the underlying molecular mechanisms. We demonstrated that AVNs treatment suppressed mitochondrial bioenergetic generation, resulting in mitochondrial swelling and increased reactive oxygen species (ROS) production. Further study indicated that AVNs treatment significantly reduced DDX3 expression, an oncogenic RNA helicase highly expressed in human CRC tissues. DDX3 overexpression reversed the ROS-mediated CRC apoptosis induced by AVNs. Of note, we identified Avenanthramide A (AVN A) as the effective ingredient in AVNs extracts. AVN A blocked the ATPase activity of DDX3 and induced its degradation by directly binding to the Arg287 and Arg294 residues in DDX3. In conclusion, these innovative findings highlight that AVNs extracts, in particular its bioactive compound AVN A may crack the current hurdles in the way of CRC treatment.</p></abstract><kwd-group kwd-group-type="npg-subject"><title>Subject terms</title><kwd>Cancer prevention</kwd><kwd>Target validation</kwd></kwd-group><funding-group><award-group><funding-source><institution>This work was supported by the National Natural Science Foundation of China (No. 31770382 and 31800657), “1331 Project” Key Innovation Center and Team of Shanxi Province (Prof. Zhuoyu Li), Shanxi Province Science Foundation for Key Projects (No. 201801D111001), Shanxi Province Science Foundation for Youths (No. 201601D021107), Scientific and Technological Innovation Programs of Higher Education Institutions in Shanxi (No. 2016121).</institution></funding-source></award-group></funding-group><custom-meta-group><custom-meta><meta-name>issue-copyright-statement</meta-name><meta-value>© The Author(s) 2019</meta-value></custom-meta></custom-meta-group></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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