Tetrandrine induces apoptosis Via caspase-8, -9, and -3 and poly (ADP ribose) polymerase dependent pathways and autophagy through beclin-1/ LC3-I, II signaling pathways in human oral cancer HSC-3 cells.
Identifieur interne : 000138 ( Main/Exploration ); précédent : 000137; suivant : 000139Tetrandrine induces apoptosis Via caspase-8, -9, and -3 and poly (ADP ribose) polymerase dependent pathways and autophagy through beclin-1/ LC3-I, II signaling pathways in human oral cancer HSC-3 cells.
Auteurs : Fu-Shun Yu [Taïwan] ; Chun-Shu Yu [Taïwan] ; Jaw-Chyun Chen [Taïwan] ; Jiun-Long Yang [Taïwan] ; Hsu-Feng Lu [Taïwan] ; Shu-Jen Chang [Taïwan] ; Meng-Wei Lin [Taïwan] ; Jing-Gung Chung [Taïwan]Source :
- Environmental toxicology [ 1522-7278 ] ; 2016.
Descripteurs français
- KwdFr :
- Apoptose (effets des médicaments et des substances chimiques), Apoptose (physiologie), Autophagie (effets des médicaments et des substances chimiques), Autophagie (physiologie), Benzylisoquinoléines (pharmacologie), Bécline-1 (MeSH), Caspase 8 (métabolisme), Caspase-3 (métabolisme), Caspase-9 (métabolisme), Fragmentation de l'ADN (MeSH), Humains (MeSH), Lignée cellulaire tumorale (MeSH), Poly(ADP-ribose) polymerases (métabolisme), Protéines associées aux microtubules (MeSH), Protéines membranaires (métabolisme), Protéines régulatrices de l'apoptose (métabolisme), Transduction du signal (MeSH), Tumeurs de la bouche (métabolisme), Tumeurs de la bouche (traitement médicamenteux).
- MESH :
- effets des médicaments et des substances chimiques : Apoptose, Autophagie.
- métabolisme : Caspase 8, Caspase-3, Caspase-9, Poly(ADP-ribose) polymerases, Protéines membranaires, Protéines régulatrices de l'apoptose, Tumeurs de la bouche.
- pharmacologie : Benzylisoquinoléines.
- physiologie : Apoptose, Autophagie.
- traitement médicamenteux : Tumeurs de la bouche.
- Bécline-1, Fragmentation de l'ADN, Humains, Lignée cellulaire tumorale, Protéines associées aux microtubules, Transduction du signal.
English descriptors
- KwdEn :
- Apoptosis (drug effects), Apoptosis (physiology), Apoptosis Regulatory Proteins (metabolism), Autophagy (drug effects), Autophagy (physiology), Beclin-1 (MeSH), Benzylisoquinolines (pharmacology), Caspase 3 (metabolism), Caspase 8 (metabolism), Caspase 9 (metabolism), Cell Line, Tumor (MeSH), DNA Fragmentation (MeSH), Humans (MeSH), Membrane Proteins (metabolism), Microtubule-Associated Proteins (MeSH), Mouth Neoplasms (drug therapy), Mouth Neoplasms (metabolism), Poly(ADP-ribose) Polymerases (metabolism), Signal Transduction (MeSH).
- MESH :
- chemical , metabolism : Apoptosis Regulatory Proteins, Caspase 3, Caspase 8, Caspase 9, Membrane Proteins, Poly(ADP-ribose) Polymerases.
- drug effects : Apoptosis, Autophagy.
- drug therapy : Mouth Neoplasms.
- metabolism : Mouth Neoplasms.
- chemical , pharmacology : Benzylisoquinolines.
- physiology : Apoptosis, Autophagy.
- chemical : Beclin-1, Cell Line, Tumor, DNA Fragmentation, Humans, Microtubule-Associated Proteins, Signal Transduction.
Abstract
Tetrandrine is a bisbenzylisoquinoline alkaloid that was found in the Radix Stephania tetrandra S Moore. It had been reported to induce cytotoxic effects on many human cancer cells. In this study, we investigated the cytotoxic effects of tetrandrine on human oral cancer HSC-3 cells in vitro. Treatments of HSC-3 cells with tetrandrine significantly decreased the percentage of viable cells through the induction of autophagy and apoptosis and these effects are in concentration-dependent manner. To define the mechanism underlying the cytotoxic effects of tetrandrine, we investigated the critical molecular events known to regulate the apoptotic and autophagic machinery. Tetrandrine induced chromatin condensation, internucleosomal DNA fragmentation, activation of caspases-3, -8, and -9, and cleavage of poly (ADP ribose) polymerase (PARP) that were associated with apoptosis, and it also enhanced the expression of LC3-I and -II that were associated with the induction of autophagy in human squamous carcinoma cell line (HSC-3) cells. Tetrandrine induced autophagy in HSC-3 cells was significantly attenuated by bafilomycin A1 (inhibitor of autophagy) pre-treatment that confirmed tetrandrine induced cell death may be associated with the autophagy. In conclusion, we suggest that tetrandrine induced cell death may be through the induction of apoptosis as well as autophagy in human oral cancer HSC-3 cells via PARP, caspases/Becline I/LC3-I/II signaling pathways.
DOI: 10.1002/tox.22053
PubMed: 25266202
Affiliations:
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sortKey="Chang, Shu Jen" sort="Chang, Shu Jen" uniqKey="Chang S" first="Shu-Jen" last="Chang">Shu-Jen Chang</name><affiliation wicri:level="1"><nlm:affiliation>School of Pharmacy, China Medical University, Taichung, 404, Taiwan.</nlm:affiliation><country xml:lang="fr">Taïwan</country><wicri:regionArea>School of Pharmacy, China Medical University, Taichung, 404</wicri:regionArea><wicri:noRegion>404</wicri:noRegion></affiliation></author><author><name sortKey="Lin, Meng Wei" sort="Lin, Meng Wei" uniqKey="Lin M" first="Meng-Wei" last="Lin">Meng-Wei Lin</name><affiliation wicri:level="1"><nlm:affiliation>Department of Nursing, Cardinal Tien Junior College of Healthcare and Management, Yilan, Taiwan.</nlm:affiliation><country xml:lang="fr">Taïwan</country><wicri:regionArea>Department of Nursing, Cardinal Tien Junior College of Healthcare and Management, Yilan</wicri:regionArea><wicri:noRegion>Yilan</wicri:noRegion></affiliation></author><author><name sortKey="Chung, Jing Gung" sort="Chung, 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404</wicri:regionArea><wicri:noRegion>404</wicri:noRegion></affiliation></author><author><name sortKey="Yu, Chun Shu" sort="Yu, Chun Shu" uniqKey="Yu C" first="Chun-Shu" last="Yu">Chun-Shu Yu</name><affiliation wicri:level="1"><nlm:affiliation>School of Pharmacy, China Medical University, Taichung, 404, Taiwan.</nlm:affiliation><country xml:lang="fr">Taïwan</country><wicri:regionArea>School of Pharmacy, China Medical University, Taichung, 404</wicri:regionArea><wicri:noRegion>404</wicri:noRegion></affiliation></author><author><name sortKey="Chen, Jaw Chyun" sort="Chen, Jaw Chyun" uniqKey="Chen J" first="Jaw-Chyun" last="Chen">Jaw-Chyun Chen</name><affiliation wicri:level="1"><nlm:affiliation>Department of Medicinal Botany and Health Applications, Da-Yeh University, Changhua, Taiwan.</nlm:affiliation><country xml:lang="fr">Taïwan</country><wicri:regionArea>Department of Medicinal Botany and Health Applications, Da-Yeh University, Changhua</wicri:regionArea><wicri:noRegion>Changhua</wicri:noRegion></affiliation></author><author><name sortKey="Yang, Jiun Long" sort="Yang, Jiun Long" uniqKey="Yang J" first="Jiun-Long" last="Yang">Jiun-Long Yang</name><affiliation wicri:level="1"><nlm:affiliation>Department of Chinese Medicine Resources, China Medical University, Taichung, 404, Taiwan.</nlm:affiliation><country xml:lang="fr">Taïwan</country><wicri:regionArea>Department of Chinese Medicine Resources, China Medical University, Taichung, 404</wicri:regionArea><wicri:noRegion>404</wicri:noRegion></affiliation></author><author><name sortKey="Lu, Hsu Feng" sort="Lu, Hsu Feng" uniqKey="Lu H" first="Hsu-Feng" last="Lu">Hsu-Feng Lu</name><affiliation wicri:level="1"><nlm:affiliation>Clinical Pathology, Cheng Hsin General Hospital, Taipei, Taiwan.</nlm:affiliation><country xml:lang="fr">Taïwan</country><wicri:regionArea>Clinical Pathology, Cheng Hsin General Hospital, Taipei</wicri:regionArea><wicri:noRegion>Taipei</wicri:noRegion></affiliation><affiliation wicri:level="1"><nlm:affiliation>School of Chinese Medicine, China Medical University, Taichung 404, Taiwan.</nlm:affiliation><country xml:lang="fr">Taïwan</country><wicri:regionArea>School of Chinese Medicine, China Medical University, Taichung 404</wicri:regionArea><wicri:noRegion>Taichung 404</wicri:noRegion></affiliation></author><author><name sortKey="Chang, Shu Jen" sort="Chang, Shu Jen" uniqKey="Chang S" first="Shu-Jen" last="Chang">Shu-Jen Chang</name><affiliation wicri:level="1"><nlm:affiliation>School of Pharmacy, China Medical University, Taichung, 404, Taiwan.</nlm:affiliation><country xml:lang="fr">Taïwan</country><wicri:regionArea>School of Pharmacy, China Medical University, Taichung, 404</wicri:regionArea><wicri:noRegion>404</wicri:noRegion></affiliation></author><author><name sortKey="Lin, Meng Wei" sort="Lin, Meng Wei" uniqKey="Lin M" first="Meng-Wei" last="Lin">Meng-Wei Lin</name><affiliation wicri:level="1"><nlm:affiliation>Department of Nursing, Cardinal Tien Junior College of Healthcare and Management, Yilan, Taiwan.</nlm:affiliation><country xml:lang="fr">Taïwan</country><wicri:regionArea>Department of Nursing, Cardinal Tien Junior College of Healthcare and Management, Yilan</wicri:regionArea><wicri:noRegion>Yilan</wicri:noRegion></affiliation></author><author><name sortKey="Chung, Jing Gung" sort="Chung, Jing Gung" uniqKey="Chung J" first="Jing-Gung" last="Chung">Jing-Gung Chung</name><affiliation wicri:level="1"><nlm:affiliation>Department of Biological Science and Technology, China Medical University, Taichung, 404, Taiwan.</nlm:affiliation><country xml:lang="fr">Taïwan</country><wicri:regionArea>Department of Biological Science and Technology, China Medical University, Taichung, 404</wicri:regionArea><wicri:noRegion>404</wicri:noRegion></affiliation><affiliation wicri:level="1"><nlm:affiliation>Department of Biotechnology, Asia University, Taichung, 413, Taiwan.</nlm:affiliation><country xml:lang="fr">Taïwan</country><wicri:regionArea>Department of Biotechnology, Asia University, Taichung, 413</wicri:regionArea><wicri:noRegion>413</wicri:noRegion></affiliation></author></analytic><series><title level="j">Environmental toxicology</title><idno type="eISSN">1522-7278</idno><imprint><date when="2016" type="published">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Apoptosis (drug effects)</term><term>Apoptosis (physiology)</term><term>Apoptosis Regulatory Proteins (metabolism)</term><term>Autophagy (drug effects)</term><term>Autophagy (physiology)</term><term>Beclin-1 (MeSH)</term><term>Benzylisoquinolines (pharmacology)</term><term>Caspase 3 (metabolism)</term><term>Caspase 8 (metabolism)</term><term>Caspase 9 (metabolism)</term><term>Cell Line, Tumor (MeSH)</term><term>DNA Fragmentation (MeSH)</term><term>Humans (MeSH)</term><term>Membrane Proteins (metabolism)</term><term>Microtubule-Associated Proteins (MeSH)</term><term>Mouth Neoplasms (drug therapy)</term><term>Mouth Neoplasms (metabolism)</term><term>Poly(ADP-ribose) Polymerases (metabolism)</term><term>Signal Transduction (MeSH)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Apoptose (effets des médicaments et des substances chimiques)</term><term>Apoptose (physiologie)</term><term>Autophagie (effets des médicaments et des substances chimiques)</term><term>Autophagie (physiologie)</term><term>Benzylisoquinoléines (pharmacologie)</term><term>Bécline-1 (MeSH)</term><term>Caspase 8 (métabolisme)</term><term>Caspase-3 (métabolisme)</term><term>Caspase-9 (métabolisme)</term><term>Fragmentation de l'ADN (MeSH)</term><term>Humains (MeSH)</term><term>Lignée cellulaire tumorale (MeSH)</term><term>Poly(ADP-ribose) polymerases (métabolisme)</term><term>Protéines associées aux microtubules (MeSH)</term><term>Protéines membranaires (métabolisme)</term><term>Protéines régulatrices de l'apoptose (métabolisme)</term><term>Transduction du signal (MeSH)</term><term>Tumeurs de la bouche (métabolisme)</term><term>Tumeurs de la bouche (traitement médicamenteux)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Apoptosis Regulatory Proteins</term><term>Caspase 3</term><term>Caspase 8</term><term>Caspase 9</term><term>Membrane Proteins</term><term>Poly(ADP-ribose) Polymerases</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Apoptosis</term><term>Autophagy</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Mouth Neoplasms</term></keywords><keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Apoptose</term><term>Autophagie</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Mouth Neoplasms</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Caspase 8</term><term>Caspase-3</term><term>Caspase-9</term><term>Poly(ADP-ribose) polymerases</term><term>Protéines membranaires</term><term>Protéines régulatrices de l'apoptose</term><term>Tumeurs de la bouche</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Benzylisoquinoléines</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Benzylisoquinolines</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Apoptose</term><term>Autophagie</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Apoptosis</term><term>Autophagy</term></keywords><keywords scheme="MESH" qualifier="traitement médicamenteux" xml:lang="fr"><term>Tumeurs de la bouche</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>Beclin-1</term><term>Cell Line, Tumor</term><term>DNA Fragmentation</term><term>Humans</term><term>Microtubule-Associated Proteins</term><term>Signal Transduction</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Bécline-1</term><term>Fragmentation de l'ADN</term><term>Humains</term><term>Lignée cellulaire tumorale</term><term>Protéines associées aux microtubules</term><term>Transduction du signal</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Tetrandrine is a bisbenzylisoquinoline alkaloid that was found in the Radix Stephania tetrandra S Moore. It had been reported to induce cytotoxic effects on many human cancer cells. In this study, we investigated the cytotoxic effects of tetrandrine on human oral cancer HSC-3 cells in vitro. Treatments of HSC-3 cells with tetrandrine significantly decreased the percentage of viable cells through the induction of autophagy and apoptosis and these effects are in concentration-dependent manner. To define the mechanism underlying the cytotoxic effects of tetrandrine, we investigated the critical molecular events known to regulate the apoptotic and autophagic machinery. Tetrandrine induced chromatin condensation, internucleosomal DNA fragmentation, activation of caspases-3, -8, and -9, and cleavage of poly (ADP ribose) polymerase (PARP) that were associated with apoptosis, and it also enhanced the expression of LC3-I and -II that were associated with the induction of autophagy in human squamous carcinoma cell line (HSC-3) cells. Tetrandrine induced autophagy in HSC-3 cells was significantly attenuated by bafilomycin A1 (inhibitor of autophagy) pre-treatment that confirmed tetrandrine induced cell death may be associated with the autophagy. In conclusion, we suggest that tetrandrine induced cell death may be through the induction of apoptosis as well as autophagy in human oral cancer HSC-3 cells via PARP, caspases/Becline I/LC3-I/II signaling pathways.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" IndexingMethod="Curated" Owner="NLM"><PMID Version="1">25266202</PMID><DateCompleted><Year>2016</Year><Month>10</Month><Day>24</Day></DateCompleted><DateRevised><Year>2021</Year><Month>09</Month><Day>10</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1522-7278</ISSN><JournalIssue CitedMedium="Internet"><Volume>31</Volume><Issue>4</Issue><PubDate><Year>2016</Year><Month>Apr</Month></PubDate></JournalIssue><Title>Environmental toxicology</Title><ISOAbbreviation>Environ Toxicol</ISOAbbreviation></Journal><ArticleTitle>Tetrandrine induces apoptosis Via caspase-8, -9, and -3 and poly (ADP ribose) polymerase dependent pathways and autophagy through beclin-1/ LC3-I, II signaling pathways in human oral cancer HSC-3 cells.</ArticleTitle><Pagination><MedlinePgn>395-406</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1002/tox.22053</ELocationID><Abstract><AbstractText>Tetrandrine is a bisbenzylisoquinoline alkaloid that was found in the Radix Stephania tetrandra S Moore. It had been reported to induce cytotoxic effects on many human cancer cells. In this study, we investigated the cytotoxic effects of tetrandrine on human oral cancer HSC-3 cells in vitro. Treatments of HSC-3 cells with tetrandrine significantly decreased the percentage of viable cells through the induction of autophagy and apoptosis and these effects are in concentration-dependent manner. To define the mechanism underlying the cytotoxic effects of tetrandrine, we investigated the critical molecular events known to regulate the apoptotic and autophagic machinery. Tetrandrine induced chromatin condensation, internucleosomal DNA fragmentation, activation of caspases-3, -8, and -9, and cleavage of poly (ADP ribose) polymerase (PARP) that were associated with apoptosis, and it also enhanced the expression of LC3-I and -II that were associated with the induction of autophagy in human squamous carcinoma cell line (HSC-3) cells. Tetrandrine induced autophagy in HSC-3 cells was significantly attenuated by bafilomycin A1 (inhibitor of autophagy) pre-treatment that confirmed tetrandrine induced cell death may be associated with the autophagy. In conclusion, we suggest that tetrandrine induced cell death may be through the induction of apoptosis as well as autophagy in human oral cancer HSC-3 cells via PARP, caspases/Becline I/LC3-I/II signaling pathways.</AbstractText><CopyrightInformation>© 2014 Wiley Periodicals, Inc.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Yu</LastName><ForeName>Fu-Shun</ForeName><Initials>FS</Initials><AffiliationInfo><Affiliation>Department of Dentist, China Medical University, Taichung, 404, Taiwan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yu</LastName><ForeName>Chun-Shu</ForeName><Initials>CS</Initials><AffiliationInfo><Affiliation>School of Pharmacy, China Medical University, Taichung, 404, Taiwan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chen</LastName><ForeName>Jaw-Chyun</ForeName><Initials>JC</Initials><AffiliationInfo><Affiliation>Department of Medicinal Botany and Health Applications, Da-Yeh University, Changhua, Taiwan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yang</LastName><ForeName>Jiun-Long</ForeName><Initials>JL</Initials><AffiliationInfo><Affiliation>Department of Chinese Medicine Resources, China Medical University, Taichung, 404, Taiwan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lu</LastName><ForeName>Hsu-Feng</ForeName><Initials>HF</Initials><AffiliationInfo><Affiliation>Clinical Pathology, Cheng Hsin General Hospital, Taipei, Taiwan.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>School of Chinese Medicine, China Medical University, Taichung 404, Taiwan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chang</LastName><ForeName>Shu-Jen</ForeName><Initials>SJ</Initials><AffiliationInfo><Affiliation>School of Pharmacy, China Medical University, Taichung, 404, Taiwan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lin</LastName><ForeName>Meng-Wei</ForeName><Initials>MW</Initials><AffiliationInfo><Affiliation>Department of Nursing, Cardinal Tien Junior College of Healthcare and Management, Yilan, Taiwan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chung</LastName><ForeName>Jing-Gung</ForeName><Initials>JG</Initials><AffiliationInfo><Affiliation>Department of Biological Science and Technology, China Medical University, Taichung, 404, Taiwan.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Biotechnology, Asia University, Taichung, 413, Taiwan.</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>2014</Year><Month>09</Month><Day>30</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Environ Toxicol</MedlineTA><NlmUniqueID>100885357</NlmUniqueID><ISSNLinking>1520-4081</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D051017">Apoptosis Regulatory Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C491997">BECN1 protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000071186">Beclin-1</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D044182">Benzylisoquinolines</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C477012">MAP1LC3A protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D008565">Membrane Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D008869">Microtubule-Associated Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>29EX23D5AJ</RegistryNumber><NameOfSubstance UI="C009438">tetrandrine</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.4.2.30</RegistryNumber><NameOfSubstance UI="D011065">Poly(ADP-ribose) Polymerases</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.4.22.-</RegistryNumber><NameOfSubstance UI="D053148">Caspase 3</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.4.22.-</RegistryNumber><NameOfSubstance UI="D053181">Caspase 8</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.4.22.-</RegistryNumber><NameOfSubstance UI="D053453">Caspase 9</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D017209" MajorTopicYN="N">Apoptosis</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051017" MajorTopicYN="N">Apoptosis Regulatory Proteins</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001343" MajorTopicYN="N">Autophagy</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000071186" MajorTopicYN="N">Beclin-1</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D044182" MajorTopicYN="N">Benzylisoquinolines</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D053148" MajorTopicYN="N">Caspase 3</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D053181" MajorTopicYN="N">Caspase 8</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D053453" MajorTopicYN="N">Caspase 9</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D045744" MajorTopicYN="N">Cell Line, Tumor</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D053938" MajorTopicYN="N">DNA Fragmentation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008565" MajorTopicYN="N">Membrane Proteins</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008869" MajorTopicYN="N">Microtubule-Associated Proteins</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009062" MajorTopicYN="N">Mouth Neoplasms</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011065" MajorTopicYN="N">Poly(ADP-ribose) Polymerases</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">HSC-3 cell line</Keyword><Keyword MajorTopicYN="N">apoptosis</Keyword><Keyword MajorTopicYN="N">autophagy</Keyword><Keyword MajorTopicYN="N">oral cancer</Keyword><Keyword MajorTopicYN="N">tetrandrine</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2014</Year><Month>06</Month><Day>02</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2014</Year><Month>09</Month><Day>05</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2014</Year><Month>09</Month><Day>10</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2014</Year><Month>10</Month><Day>1</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2014</Year><Month>10</Month><Day>1</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2016</Year><Month>10</Month><Day>25</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">25266202</ArticleId><ArticleId IdType="doi">10.1002/tox.22053</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Taïwan</li></country></list><tree><country name="Taïwan"><noRegion><name sortKey="Yu, Fu Shun" sort="Yu, Fu Shun" uniqKey="Yu F" first="Fu-Shun" last="Yu">Fu-Shun Yu</name></noRegion><name sortKey="Chang, Shu Jen" sort="Chang, Shu Jen" uniqKey="Chang S" first="Shu-Jen" last="Chang">Shu-Jen Chang</name><name sortKey="Chen, Jaw Chyun" sort="Chen, Jaw Chyun" uniqKey="Chen J" first="Jaw-Chyun" last="Chen">Jaw-Chyun Chen</name><name sortKey="Chung, Jing Gung" sort="Chung, Jing Gung" uniqKey="Chung J" first="Jing-Gung" last="Chung">Jing-Gung Chung</name><name sortKey="Chung, Jing Gung" sort="Chung, Jing Gung" uniqKey="Chung J" first="Jing-Gung" last="Chung">Jing-Gung Chung</name><name sortKey="Lin, Meng Wei" sort="Lin, Meng Wei" uniqKey="Lin M" first="Meng-Wei" last="Lin">Meng-Wei Lin</name><name sortKey="Lu, Hsu Feng" sort="Lu, Hsu Feng" uniqKey="Lu H" first="Hsu-Feng" last="Lu">Hsu-Feng Lu</name><name sortKey="Lu, Hsu Feng" sort="Lu, Hsu Feng" uniqKey="Lu H" first="Hsu-Feng" last="Lu">Hsu-Feng Lu</name><name sortKey="Yang, Jiun Long" sort="Yang, Jiun Long" uniqKey="Yang J" first="Jiun-Long" last="Yang">Jiun-Long Yang</name><name sortKey="Yu, Chun Shu" sort="Yu, Chun Shu" uniqKey="Yu C" first="Chun-Shu" last="Yu">Chun-Shu Yu</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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|texte= Tetrandrine induces apoptosis Via caspase-8, -9, and -3 and poly (ADP ribose) polymerase dependent pathways and autophagy through beclin-1/ LC3-I, II signaling pathways in human oral cancer HSC-3 cells.
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