Paris Saponin II induced apoptosis via activation of autophagy in human lung cancer cells.
Identifieur interne : 000208 ( PubMed/Corpus ); précédent : 000207; suivant : 000209Paris Saponin II induced apoptosis via activation of autophagy in human lung cancer cells.
Auteurs : Lili Zhang ; Shuli Man ; Yongshuai Wang ; Jing Liu ; Zhen Liu ; Peng Yu ; Wenyuan GaoSource :
- Chemico-biological interactions [ 1872-7786 ] ; 2016.
English descriptors
- KwdEn :
- A549 Cells, Acetylcysteine (pharmacology), Apoptosis (drug effects), Autophagy (drug effects), Blotting, Western, Cell Line, Chloroquine (toxicity), Glutathione (metabolism), Humans, JNK Mitogen-Activated Protein Kinases (metabolism), Lung Neoplasms (metabolism), Lung Neoplasms (pathology), Microscopy, Electron, Transmission, Microscopy, Fluorescence, Phosphatidylinositol 3-Kinases (metabolism), Proto-Oncogene Proteins c-akt (metabolism), Reactive Oxygen Species (metabolism), Rhizome (chemistry), Rhizome (metabolism), Saponins (pharmacology), Signal Transduction (drug effects).
- MESH :
- chemical , metabolism : Glutathione, JNK Mitogen-Activated Protein Kinases, Phosphatidylinositol 3-Kinases, Proto-Oncogene Proteins c-akt, Reactive Oxygen Species.
- chemical , pharmacology : Acetylcysteine, Saponins.
- chemistry : Rhizome.
- drug effects : Apoptosis, Autophagy, Signal Transduction.
- metabolism : Lung Neoplasms, Rhizome.
- pathology : Lung Neoplasms.
- chemical , toxicity : Chloroquine.
- A549 Cells, Blotting, Western, Cell Line, Humans, Microscopy, Electron, Transmission, Microscopy, Fluorescence.
Abstract
Paris Saponin II (PSII) has been shown anticancer activity against several cancer lines through the pro-apoptotic pathway. The aim of the study was to investigate the relationship between apoptosis and autophagy taking part in the anti-cancer mechanisms of PSII. In this study, PSII induced autophagy and apoptosis in dose- and time-dependent manners. Meanwhile, it induced autophagy as early as 2 h after exposure to 1 μM of PSII accompanying with apoptosis. Blockade of autophagy with chloroquine (CQ) attenuated apoptosis, while regulation of reactive oxygen species (ROS) by N-acetyl cysteine (NAC), gallic acid (GA) and H2O2 could not influence autophagy. In addition, PSII induced apoptosis via activation of autophagy, which might be associated with the activation of JNK and inhibition of PI3K/AKT/mTOR pathway. All in all, our research increased the understanding of the role of PSII regulating autophagy and apoptosis, which would hopefully provide prospective strategies for cancer therapy.
DOI: 10.1016/j.cbi.2016.05.016
PubMed: 27180204
Links to Exploration step
pubmed:27180204Le document en format XML
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Electronic address: msl@tust.edu.cn.</nlm:affiliation></affiliation></author><author><name sortKey="Wang, Yongshuai" sort="Wang, Yongshuai" uniqKey="Wang Y" first="Yongshuai" last="Wang">Yongshuai Wang</name><affiliation><nlm:affiliation>Key Laboratory of Industrial Microbiology, Ministry of Education, College of Biotechnology, Tianjin University of Science & Technology, Tianjin, 300457, China.</nlm:affiliation></affiliation></author><author><name sortKey="Liu, Jing" sort="Liu, Jing" uniqKey="Liu J" first="Jing" last="Liu">Jing Liu</name><affiliation><nlm:affiliation>Key Laboratory of Industrial Microbiology, Ministry of Education, College of Biotechnology, Tianjin University of Science & Technology, Tianjin, 300457, China.</nlm:affiliation></affiliation></author><author><name sortKey="Liu, Zhen" sort="Liu, Zhen" uniqKey="Liu Z" first="Zhen" last="Liu">Zhen Liu</name><affiliation><nlm:affiliation>Key Laboratory of Industrial Microbiology, Ministry of Education, College of Biotechnology, Tianjin University of Science & Technology, Tianjin, 300457, China.</nlm:affiliation></affiliation></author><author><name sortKey="Yu, Peng" sort="Yu, Peng" uniqKey="Yu P" first="Peng" last="Yu">Peng Yu</name><affiliation><nlm:affiliation>Key Laboratory of Industrial Microbiology, Ministry of Education, College of Biotechnology, Tianjin University of Science & Technology, Tianjin, 300457, China.</nlm:affiliation></affiliation></author><author><name sortKey="Gao, Wenyuan" sort="Gao, Wenyuan" uniqKey="Gao W" first="Wenyuan" last="Gao">Wenyuan Gao</name><affiliation><nlm:affiliation>Tianjin Key Laboratory for Modern Drug Delivery and High Efficiency, School of Pharmaceutical Science and Technology, Tianjin University, Tianjin, 300072, China. 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Electronic address: msl@tust.edu.cn.</nlm:affiliation></affiliation></author><author><name sortKey="Wang, Yongshuai" sort="Wang, Yongshuai" uniqKey="Wang Y" first="Yongshuai" last="Wang">Yongshuai Wang</name><affiliation><nlm:affiliation>Key Laboratory of Industrial Microbiology, Ministry of Education, College of Biotechnology, Tianjin University of Science & Technology, Tianjin, 300457, China.</nlm:affiliation></affiliation></author><author><name sortKey="Liu, Jing" sort="Liu, Jing" uniqKey="Liu J" first="Jing" last="Liu">Jing Liu</name><affiliation><nlm:affiliation>Key Laboratory of Industrial Microbiology, Ministry of Education, College of Biotechnology, Tianjin University of Science & Technology, Tianjin, 300457, China.</nlm:affiliation></affiliation></author><author><name sortKey="Liu, Zhen" sort="Liu, Zhen" uniqKey="Liu Z" first="Zhen" last="Liu">Zhen Liu</name><affiliation><nlm:affiliation>Key Laboratory of Industrial Microbiology, Ministry of Education, College of Biotechnology, Tianjin University of Science & Technology, Tianjin, 300457, China.</nlm:affiliation></affiliation></author><author><name sortKey="Yu, Peng" sort="Yu, Peng" uniqKey="Yu P" first="Peng" last="Yu">Peng Yu</name><affiliation><nlm:affiliation>Key Laboratory of Industrial Microbiology, Ministry of Education, College of Biotechnology, Tianjin University of Science & Technology, Tianjin, 300457, China.</nlm:affiliation></affiliation></author><author><name sortKey="Gao, Wenyuan" sort="Gao, Wenyuan" uniqKey="Gao W" first="Wenyuan" last="Gao">Wenyuan Gao</name><affiliation><nlm:affiliation>Tianjin Key Laboratory for Modern Drug Delivery and High Efficiency, School of Pharmaceutical Science and Technology, Tianjin University, Tianjin, 300072, China. Electronic address: biochemgao@163.com.</nlm:affiliation></affiliation></author></analytic><series><title level="j">Chemico-biological interactions</title><idno type="eISSN">1872-7786</idno><imprint><date when="2016" type="published">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>A549 Cells</term><term>Acetylcysteine (pharmacology)</term><term>Apoptosis (drug effects)</term><term>Autophagy (drug effects)</term><term>Blotting, Western</term><term>Cell Line</term><term>Chloroquine (toxicity)</term><term>Glutathione (metabolism)</term><term>Humans</term><term>JNK Mitogen-Activated Protein Kinases (metabolism)</term><term>Lung Neoplasms (metabolism)</term><term>Lung Neoplasms (pathology)</term><term>Microscopy, Electron, Transmission</term><term>Microscopy, Fluorescence</term><term>Phosphatidylinositol 3-Kinases (metabolism)</term><term>Proto-Oncogene Proteins c-akt (metabolism)</term><term>Reactive Oxygen Species (metabolism)</term><term>Rhizome (chemistry)</term><term>Rhizome (metabolism)</term><term>Saponins (pharmacology)</term><term>Signal Transduction (drug effects)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Glutathione</term><term>JNK Mitogen-Activated Protein Kinases</term><term>Phosphatidylinositol 3-Kinases</term><term>Proto-Oncogene Proteins c-akt</term><term>Reactive Oxygen Species</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Acetylcysteine</term><term>Saponins</term></keywords><keywords scheme="MESH" qualifier="chemistry" xml:lang="en"><term>Rhizome</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Apoptosis</term><term>Autophagy</term><term>Signal Transduction</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Lung Neoplasms</term><term>Rhizome</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Lung Neoplasms</term></keywords><keywords scheme="MESH" type="chemical" qualifier="toxicity" xml:lang="en"><term>Chloroquine</term></keywords><keywords scheme="MESH" xml:lang="en"><term>A549 Cells</term><term>Blotting, Western</term><term>Cell Line</term><term>Humans</term><term>Microscopy, Electron, Transmission</term><term>Microscopy, Fluorescence</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Paris Saponin II (PSII) has been shown anticancer activity against several cancer lines through the pro-apoptotic pathway. The aim of the study was to investigate the relationship between apoptosis and autophagy taking part in the anti-cancer mechanisms of PSII. In this study, PSII induced autophagy and apoptosis in dose- and time-dependent manners. Meanwhile, it induced autophagy as early as 2 h after exposure to 1 μM of PSII accompanying with apoptosis. Blockade of autophagy with chloroquine (CQ) attenuated apoptosis, while regulation of reactive oxygen species (ROS) by N-acetyl cysteine (NAC), gallic acid (GA) and H2O2 could not influence autophagy. In addition, PSII induced apoptosis via activation of autophagy, which might be associated with the activation of JNK and inhibition of PI3K/AKT/mTOR pathway. All in all, our research increased the understanding of the role of PSII regulating autophagy and apoptosis, which would hopefully provide prospective strategies for cancer therapy. </div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">27180204</PMID><DateCompleted><Year>2017</Year><Month>01</Month><Day>30</Day></DateCompleted><DateRevised><Year>2017</Year><Month>01</Month><Day>30</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1872-7786</ISSN><JournalIssue CitedMedium="Internet"><Volume>253</Volume><PubDate><Year>2016</Year><Month>Jun</Month><Day>25</Day></PubDate></JournalIssue><Title>Chemico-biological interactions</Title><ISOAbbreviation>Chem. Biol. Interact.</ISOAbbreviation></Journal><ArticleTitle>Paris Saponin II induced apoptosis via activation of autophagy in human lung cancer cells.</ArticleTitle><Pagination><MedlinePgn>125-33</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.cbi.2016.05.016</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S0009-2797(16)30186-7</ELocationID><Abstract><AbstractText>Paris Saponin II (PSII) has been shown anticancer activity against several cancer lines through the pro-apoptotic pathway. The aim of the study was to investigate the relationship between apoptosis and autophagy taking part in the anti-cancer mechanisms of PSII. In this study, PSII induced autophagy and apoptosis in dose- and time-dependent manners. Meanwhile, it induced autophagy as early as 2 h after exposure to 1 μM of PSII accompanying with apoptosis. Blockade of autophagy with chloroquine (CQ) attenuated apoptosis, while regulation of reactive oxygen species (ROS) by N-acetyl cysteine (NAC), gallic acid (GA) and H2O2 could not influence autophagy. In addition, PSII induced apoptosis via activation of autophagy, which might be associated with the activation of JNK and inhibition of PI3K/AKT/mTOR pathway. All in all, our research increased the understanding of the role of PSII regulating autophagy and apoptosis, which would hopefully provide prospective strategies for cancer therapy. </AbstractText><CopyrightInformation>Copyright © 2016 Elsevier Ireland Ltd. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Lili</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Key Laboratory of Industrial Microbiology, Ministry of Education, College of Biotechnology, Tianjin University of Science & Technology, Tianjin, 300457, China; Tianjin Key Laboratory of Industry Microbiology, College of Biotechnology, Tianjin University of Science & Technology, Tianjin, 300457, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Man</LastName><ForeName>Shuli</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Key Laboratory of Industrial Microbiology, Ministry of Education, College of Biotechnology, Tianjin University of Science & Technology, Tianjin, 300457, China; Tianjin Key Laboratory of Industry Microbiology, College of Biotechnology, Tianjin University of Science & Technology, Tianjin, 300457, China. Electronic address: msl@tust.edu.cn.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Yongshuai</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Key Laboratory of Industrial Microbiology, Ministry of Education, College of Biotechnology, Tianjin University of Science & Technology, Tianjin, 300457, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Jing</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Key Laboratory of Industrial Microbiology, Ministry of Education, College of Biotechnology, Tianjin University of Science & Technology, Tianjin, 300457, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Zhen</ForeName><Initials>Z</Initials><AffiliationInfo><Affiliation>Key Laboratory of Industrial Microbiology, Ministry of Education, College of Biotechnology, Tianjin University of Science & Technology, Tianjin, 300457, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yu</LastName><ForeName>Peng</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Key Laboratory of Industrial Microbiology, Ministry of Education, College of Biotechnology, Tianjin University of Science & Technology, Tianjin, 300457, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gao</LastName><ForeName>Wenyuan</ForeName><Initials>W</Initials><AffiliationInfo><Affiliation>Tianjin Key Laboratory for Modern Drug Delivery and High Efficiency, School of Pharmaceutical Science and Technology, Tianjin University, Tianjin, 300072, China. Electronic address: biochemgao@163.com.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2016</Year><Month>05</Month><Day>11</Day></ArticleDate></Article><MedlineJournalInfo><Country>Ireland</Country><MedlineTA>Chem Biol Interact</MedlineTA><NlmUniqueID>0227276</NlmUniqueID><ISSNLinking>0009-2797</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D017382">Reactive Oxygen Species</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D012503">Saponins</NameOfSubstance></Chemical><Chemical><RegistryNumber>886U3H6UFF</RegistryNumber><NameOfSubstance UI="D002738">Chloroquine</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.1.-</RegistryNumber><NameOfSubstance UI="D019869">Phosphatidylinositol 3-Kinases</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.11.1</RegistryNumber><NameOfSubstance UI="D051057">Proto-Oncogene Proteins c-akt</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.11.24</RegistryNumber><NameOfSubstance UI="D048031">JNK Mitogen-Activated Protein Kinases</NameOfSubstance></Chemical><Chemical><RegistryNumber>GAN16C9B8O</RegistryNumber><NameOfSubstance UI="D005978">Glutathione</NameOfSubstance></Chemical><Chemical><RegistryNumber>WYQ7N0BPYC</RegistryNumber><NameOfSubstance UI="D000111">Acetylcysteine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000072283" MajorTopicYN="N">A549 Cells</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000111" MajorTopicYN="N">Acetylcysteine</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017209" MajorTopicYN="N">Apoptosis</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001343" MajorTopicYN="N">Autophagy</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015153" MajorTopicYN="N">Blotting, Western</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002460" MajorTopicYN="N">Cell Line</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002738" MajorTopicYN="N">Chloroquine</DescriptorName><QualifierName UI="Q000633" MajorTopicYN="N">toxicity</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005978" MajorTopicYN="N">Glutathione</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D048031" 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MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017382" MajorTopicYN="N">Reactive Oxygen Species</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D027343" MajorTopicYN="N">Rhizome</DescriptorName><QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012503" MajorTopicYN="N">Saponins</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Apoptosis</Keyword><Keyword MajorTopicYN="N">Autophagy</Keyword><Keyword MajorTopicYN="N">Paris Saponin II</Keyword><Keyword MajorTopicYN="N">ROS</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2016</Year><Month>02</Month><Day>19</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2016</Year><Month>05</Month><Day>06</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2016</Year><Month>05</Month><Day>10</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2016</Year><Month>5</Month><Day>16</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2016</Year><Month>5</Month><Day>18</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2017</Year><Month>1</Month><Day>31</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">27180204</ArticleId><ArticleId IdType="pii">S0009-2797(16)30186-7</ArticleId><ArticleId 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