Sotetsuflavone Induces Autophagy in Non-Small Cell Lung Cancer Through Blocking PI3K/Akt/mTOR Signaling Pathway in Vivo and in Vitro
Identifieur interne : 000575 ( Pmc/Curation ); précédent : 000574; suivant : 000576Sotetsuflavone Induces Autophagy in Non-Small Cell Lung Cancer Through Blocking PI3K/Akt/mTOR Signaling Pathway in Vivo and in Vitro
Auteurs : Shaohui Wang [République populaire de Chine] ; Xiaoling Xu [République populaire de Chine] ; Yanlan Hu [République populaire de Chine] ; Tao Lei [République populaire de Chine] ; Tongxiang Liu [République populaire de Chine]Source :
- Frontiers in Pharmacology [ 1663-9812 ] ; 2019.
Abstract
Non-small cell lung cancer (NSCLC) is a globally scaled disease with a high incidence and high associated mortality rate. Autophagy is one of the important physiological activities that helps to control cell survival, influences the dynamics of cell death, and which plays a crucial role in the pathophysiology of NSCLC. Sotetsuflavone is a naturally derived and occurring flavonoid, and previous studies have demonstrated that sotetsuflavone possesses potential anti-cancer activities. However, whether or not sotetsuflavone induces autophagy, as well as has effects and influences cell death in NSCLC cells remains unclear. Thus, in our study, we examined and elucidated the roles and underlying mechanisms of sotetsuflavone upon the dynamics of autophagy in NSCLC
Url:
DOI: 10.3389/fphar.2019.01460
PubMed: 31920653
PubMed Central: 6915081
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nlm:aff country strict</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="aff3"><institution>School of Pharmacy, Minzu University of China</institution>,<addr-line>Beijing</addr-line>,<country>China</country></nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author><author><name sortKey="Xu, Xiaoling" sort="Xu, Xiaoling" uniqKey="Xu X" first="Xiaoling" last="Xu">Xiaoling Xu</name><affiliation wicri:level="1"><nlm:aff id="aff4"><institution>Department of Medical Oncology, Institute of Cancer Research and Basic Medical Sciences of Chinese Academy of Sciences, Cancer Hospital of University of Chinese Academy of Sciences, Zhejiang Cancer Hospital</institution>,<addr-line>Hangzhou</addr-line>,<country>China</country></nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author><author><name sortKey="Hu, Yanlan" sort="Hu, Yanlan" uniqKey="Hu Y" first="Yanlan" last="Hu">Yanlan Hu</name><affiliation wicri:level="1"><nlm:aff id="aff1"><institution>Key Laboratory of Ethnomedicine (Minzu University of China), Minority of Education</institution>,<addr-line>Beijing</addr-line>,<country>China</country></nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="aff3"><institution>School of Pharmacy, Minzu University of China</institution>,<addr-line>Beijing</addr-line>,<country>China</country></nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author><author><name sortKey="Lei, Tao" sort="Lei, Tao" uniqKey="Lei T" first="Tao" last="Lei">Tao Lei</name><affiliation wicri:level="1"><nlm:aff 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id="aff3"><institution>School of Pharmacy, Minzu University of China</institution>,<addr-line>Beijing</addr-line>,<country>China</country></nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">31920653</idno><idno type="pmc">6915081</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6915081</idno><idno type="RBID">PMC:6915081</idno><idno type="doi">10.3389/fphar.2019.01460</idno><date when="2019">2019</date><idno type="wicri:Area/Pmc/Corpus">000575</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000575</idno><idno type="wicri:Area/Pmc/Curation">000575</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Curation">000575</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Sotetsuflavone Induces Autophagy in Non-Small Cell Lung Cancer Through Blocking PI3K/Akt/mTOR Signaling Pathway <italic>in Vivo</italic> and <italic>in Vitro</italic></title><author><name sortKey="Wang, Shaohui" sort="Wang, Shaohui" uniqKey="Wang S" first="Shaohui" last="Wang">Shaohui Wang</name><affiliation wicri:level="1"><nlm:aff id="aff1"><institution>Key Laboratory of Ethnomedicine (Minzu University of China), Minority of Education</institution>,<addr-line>Beijing</addr-line>,<country>China</country></nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="aff2"><institution>Medical College, Qingdao Binhai University</institution>,<addr-line>Qingdao</addr-line>,<country>China</country></nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="aff3"><institution>School of Pharmacy, Minzu University of China</institution>,<addr-line>Beijing</addr-line>,<country>China</country></nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author><author><name sortKey="Xu, Xiaoling" sort="Xu, Xiaoling" uniqKey="Xu X" first="Xiaoling" last="Xu">Xiaoling Xu</name><affiliation wicri:level="1"><nlm:aff id="aff4"><institution>Department of Medical Oncology, Institute of Cancer Research and Basic Medical Sciences of Chinese Academy of Sciences, Cancer Hospital of University of Chinese Academy of Sciences, Zhejiang Cancer Hospital</institution>,<addr-line>Hangzhou</addr-line>,<country>China</country></nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author><author><name sortKey="Hu, Yanlan" sort="Hu, Yanlan" uniqKey="Hu Y" first="Yanlan" last="Hu">Yanlan Hu</name><affiliation wicri:level="1"><nlm:aff id="aff1"><institution>Key Laboratory of Ethnomedicine (Minzu University of China), Minority of Education</institution>,<addr-line>Beijing</addr-line>,<country>China</country></nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="aff3"><institution>School of Pharmacy, Minzu University of China</institution>,<addr-line>Beijing</addr-line>,<country>China</country></nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author><author><name sortKey="Lei, Tao" sort="Lei, Tao" uniqKey="Lei T" first="Tao" last="Lei">Tao Lei</name><affiliation wicri:level="1"><nlm:aff id="aff4"><institution>Department of Medical Oncology, Institute of Cancer Research and Basic Medical Sciences of Chinese Academy of Sciences, Cancer Hospital of University of Chinese Academy of Sciences, Zhejiang Cancer Hospital</institution>,<addr-line>Hangzhou</addr-line>,<country>China</country></nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author><author><name sortKey="Liu, Tongxiang" sort="Liu, Tongxiang" uniqKey="Liu T" first="Tongxiang" last="Liu">Tongxiang Liu</name><affiliation wicri:level="1"><nlm:aff id="aff1"><institution>Key Laboratory of Ethnomedicine (Minzu University of China), Minority of Education</institution>,<addr-line>Beijing</addr-line>,<country>China</country></nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="aff3"><institution>School of Pharmacy, Minzu University of China</institution>,<addr-line>Beijing</addr-line>,<country>China</country></nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author></analytic><series><title level="j">Frontiers in Pharmacology</title><idno type="eISSN">1663-9812</idno><imprint><date when="2019">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Non-small cell lung cancer (NSCLC) is a globally scaled disease with a high incidence and high associated mortality rate. Autophagy is one of the important physiological activities that helps to control cell survival, influences the dynamics of cell death, and which plays a crucial role in the pathophysiology of NSCLC. Sotetsuflavone is a naturally derived and occurring flavonoid, and previous studies have demonstrated that sotetsuflavone possesses potential anti-cancer activities. However, whether or not sotetsuflavone induces autophagy, as well as has effects and influences cell death in NSCLC cells remains unclear. Thus, in our study, we examined and elucidated the roles and underlying mechanisms of sotetsuflavone upon the dynamics of autophagy in NSCLC <italic>in vivo</italic> and <italic>in vitro</italic>. The results indicated that sotetsuflavone was able to inhibit proliferation, migration, and invasion of NSCLC cells. Mechanistically, sotetsuflavone was able to induce apoptosis by increasing the levels of expression of cytochrome C, cleaved-caspase 3, cleaved-caspase 9, and Bax, and contrastingly decreased levels of expression of Bcl-2. In addition, we also found that decreased levels of expression of cyclin D1 and CDK4 caused arrest of the G0/G1 phases of the cell cycle. Furthermore, we also found that sotetsuflavone could induce autophagy which in turn can play a cytoprotective effect on apoptosis in NSCLC. Sotetsuflavone-induced autophagy appeared related to the blocking of the PI3K/Akt/mTOR pathway. Our <italic>in vivo</italic> study demonstrated that sotetsuflavone significantly inhibited the growth of xenograft model inoculated A549 tumor with high a degree of safety. Taken together, these findings suggest that sotetsuflavone induces autophagy in NSCLC cells through its effects upon blocking of the PI3K/Akt/mTOR signaling pathways. Our study may provide a theoretical basis for future clinical applications of sotetsuflavone and its use as a chemotherapeutic agent for treatment of NSCLC.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct></biblStruct><biblStruct><analytic><author><name sortKey="Aryal, P" uniqKey="Aryal P">P. Aryal</name></author><author><name sortKey="Kim, K" uniqKey="Kim K">K. Kim</name></author><author><name sortKey="Park, P H" uniqKey="Park P">P. H. Park</name></author><author><name sortKey="Ham, S" uniqKey="Ham S">S. Ham</name></author><author><name sortKey="Cho, J" uniqKey="Cho J">J. Cho</name></author><author><name sortKey="Song, K" uniqKey="Song K">K. Song</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Ashwell, M A" uniqKey="Ashwell M">M. A. Ashwell</name></author><author><name sortKey="Lapierre, J M" uniqKey="Lapierre J">J. M. Lapierre</name></author><author><name sortKey="Brassard, C" uniqKey="Brassard C">C. 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<front><journal-meta><journal-id journal-id-type="nlm-ta">Front Pharmacol</journal-id><journal-id journal-id-type="iso-abbrev">Front Pharmacol</journal-id><journal-id journal-id-type="publisher-id">Front. Pharmacol.</journal-id><journal-title-group><journal-title>Frontiers in Pharmacology</journal-title></journal-title-group><issn pub-type="epub">1663-9812</issn><publisher><publisher-name>Frontiers Media S.A.</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">31920653</article-id><article-id pub-id-type="pmc">6915081</article-id><article-id pub-id-type="doi">10.3389/fphar.2019.01460</article-id><article-categories><subj-group subj-group-type="heading"><subject>Pharmacology</subject><subj-group><subject>Original Research</subject></subj-group></subj-group></article-categories><title-group><article-title>Sotetsuflavone Induces Autophagy in Non-Small Cell Lung Cancer Through Blocking PI3K/Akt/mTOR Signaling Pathway <italic>in Vivo</italic> and <italic>in Vitro</italic></article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Wang</surname><given-names>Shaohui</given-names></name><xref ref-type="aff" rid="aff1"><sup>1</sup></xref><xref ref-type="aff" rid="aff2"><sup>2</sup></xref><xref ref-type="aff" rid="aff3"><sup>3</sup></xref><xref ref-type="author-notes" rid="fn001"><sup>*</sup></xref><uri xlink:type="simple" xlink:href="https://loop.frontiersin.org/people/784740"></uri></contrib><contrib contrib-type="author"><name><surname>Xu</surname><given-names>Xiaoling</given-names></name><xref ref-type="aff" rid="aff4"><sup>4</sup></xref></contrib><contrib contrib-type="author"><name><surname>Hu</surname><given-names>Yanlan</given-names></name><xref ref-type="aff" rid="aff1"><sup>1</sup></xref><xref ref-type="aff" rid="aff3"><sup>3</sup></xref></contrib><contrib contrib-type="author"><name><surname>Lei</surname><given-names>Tao</given-names></name><xref ref-type="aff" rid="aff4"><sup>4</sup></xref></contrib><contrib contrib-type="author"><name><surname>Liu</surname><given-names>Tongxiang</given-names></name><xref ref-type="aff" rid="aff1"><sup>1</sup></xref><xref ref-type="aff" rid="aff3"><sup>3</sup></xref><xref ref-type="author-notes" rid="fn001"><sup>*</sup></xref><uri xlink:type="simple" xlink:href="https://loop.frontiersin.org/people/788981"></uri></contrib></contrib-group><aff id="aff1"><sup>1</sup><institution>Key Laboratory of Ethnomedicine (Minzu University of China), Minority of Education</institution>,<addr-line>Beijing</addr-line>,<country>China</country></aff><aff id="aff2"><sup>2</sup><institution>Medical College, Qingdao Binhai University</institution>,<addr-line>Qingdao</addr-line>,<country>China</country></aff><aff id="aff3"><sup>3</sup><institution>School of Pharmacy, Minzu University of China</institution>,<addr-line>Beijing</addr-line>,<country>China</country></aff><aff id="aff4"><sup>4</sup><institution>Department of Medical Oncology, Institute of Cancer Research and Basic Medical Sciences of Chinese Academy of Sciences, Cancer Hospital of University of Chinese Academy of Sciences, Zhejiang Cancer Hospital</institution>,<addr-line>Hangzhou</addr-line>,<country>China</country></aff><author-notes><fn fn-type="edited-by"><p>Edited by: Suresh Kumar, University of New Mexico, United States</p></fn><fn fn-type="edited-by"><p>Reviewed by: Prashant Nighot, Pennsylvania State University, United States; Agnieszka Zdzisława Robaszkiewicz, University of Łódź, Poland</p></fn><corresp id="fn001">*Correspondence: Shaohui Wang, <email xlink:href="mailto:winter9091@163.com" xlink:type="simple">winter9091@163.com</email>; Tongxiang Liu, <email xlink:href="mailto:tongxliu123@hotmail.com" xlink:type="simple">tongxliu123@hotmail.com</email></corresp><fn fn-type="other" id="fn002"><p>This article was submitted to Pharmacology of Anti-Cancer Drugs, a section of the journal Frontiers in Pharmacology</p></fn></author-notes><pub-date pub-type="epub"><day>05</day><month>12</month><year>2019</year></pub-date><pub-date pub-type="collection"><year>2019</year></pub-date><volume>10</volume><elocation-id>1460</elocation-id><history><date date-type="received"><day>06</day><month>9</month><year>2019</year></date><date date-type="accepted"><day>13</day><month>11</month><year>2019</year></date></history><permissions><copyright-statement>Copyright © 2019 Wang, Xu, Hu, Lei and Liu</copyright-statement><copyright-year>2019</copyright-year><copyright-holder>Wang, Xu, Hu, Lei and Liu</copyright-holder><license xlink:href="http://creativecommons.org/licenses/by/4.0/"><license-p>This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.</license-p></license></permissions><abstract><p>Non-small cell lung cancer (NSCLC) is a globally scaled disease with a high incidence and high associated mortality rate. Autophagy is one of the important physiological activities that helps to control cell survival, influences the dynamics of cell death, and which plays a crucial role in the pathophysiology of NSCLC. Sotetsuflavone is a naturally derived and occurring flavonoid, and previous studies have demonstrated that sotetsuflavone possesses potential anti-cancer activities. However, whether or not sotetsuflavone induces autophagy, as well as has effects and influences cell death in NSCLC cells remains unclear. Thus, in our study, we examined and elucidated the roles and underlying mechanisms of sotetsuflavone upon the dynamics of autophagy in NSCLC <italic>in vivo</italic> and <italic>in vitro</italic>. The results indicated that sotetsuflavone was able to inhibit proliferation, migration, and invasion of NSCLC cells. Mechanistically, sotetsuflavone was able to induce apoptosis by increasing the levels of expression of cytochrome C, cleaved-caspase 3, cleaved-caspase 9, and Bax, and contrastingly decreased levels of expression of Bcl-2. In addition, we also found that decreased levels of expression of cyclin D1 and CDK4 caused arrest of the G0/G1 phases of the cell cycle. Furthermore, we also found that sotetsuflavone could induce autophagy which in turn can play a cytoprotective effect on apoptosis in NSCLC. Sotetsuflavone-induced autophagy appeared related to the blocking of the PI3K/Akt/mTOR pathway. Our <italic>in vivo</italic> study demonstrated that sotetsuflavone significantly inhibited the growth of xenograft model inoculated A549 tumor with high a degree of safety. Taken together, these findings suggest that sotetsuflavone induces autophagy in NSCLC cells through its effects upon blocking of the PI3K/Akt/mTOR signaling pathways. Our study may provide a theoretical basis for future clinical applications of sotetsuflavone and its use as a chemotherapeutic agent for treatment of NSCLC.</p></abstract><kwd-group><kwd>sotetsuflavone</kwd><kwd>non-small cell lung cancer</kwd><kwd>apoptosis</kwd><kwd>autophagy</kwd><kwd>PI3K/Akt/mTOR signaling pathway</kwd></kwd-group><counts><fig-count count="7"></fig-count><table-count count="0"></table-count><equation-count count="0"></equation-count><ref-count count="46"></ref-count><page-count count="15"></page-count><word-count count="7511"></word-count></counts></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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