Anti-Cancerous Effect of Inonotus taiwanensis Polysaccharide Extract on Human Acute Monocytic Leukemia Cells through ROS-Independent Intrinsic Mitochondrial Pathway.
Identifieur interne : 000660 ( Main/Exploration ); précédent : 000659; suivant : 000661Anti-Cancerous Effect of Inonotus taiwanensis Polysaccharide Extract on Human Acute Monocytic Leukemia Cells through ROS-Independent Intrinsic Mitochondrial Pathway.
Auteurs : Tsai-Ling Chao [Taïwan] ; Ting-Yin Wang [Taïwan] ; Chin-Huei Lee [Taïwan] ; Shuenn-Jiun Yiin [Taïwan] ; Chun-Te Ho [Taïwan] ; Sheng-Hua Wu [Taïwan] ; Huey-Ling You [Taïwan] ; Chi-Liang Chern [Taïwan]Source :
- International journal of molecular sciences [ 1422-0067 ] ; 2018.
Descripteurs français
- KwdFr :
- Acétylcystéine (pharmacologie), Antinéoplasiques (pharmacologie), Apoptose (MeSH), Autophagie (MeSH), Basidiomycota (composition chimique), Endodeoxyribonucleases (métabolisme), Espèces réactives de l'oxygène (métabolisme), Fragmentation de l'ADN (MeSH), Humains (MeSH), Inhibiteurs des caspases (pharmacologie), Leucémie myéloïde (métabolisme), Lignée cellulaire tumorale (MeSH), Mitochondries (effets des médicaments et des substances chimiques), Mitochondries (métabolisme), Monocytes (effets des médicaments et des substances chimiques), Monocytes (métabolisme), Polysaccharides fongiques (pharmacologie), Potentiel de membrane mitochondriale (MeSH).
- MESH :
- composition chimique : Basidiomycota.
- effets des médicaments et des substances chimiques : Mitochondries, Monocytes.
- métabolisme : Endodeoxyribonucleases, Espèces réactives de l'oxygène, Leucémie myéloïde, Mitochondries, Monocytes.
- pharmacologie : Acétylcystéine, Antinéoplasiques, Inhibiteurs des caspases, Polysaccharides fongiques.
- Apoptose, Autophagie, Fragmentation de l'ADN, Humains, Lignée cellulaire tumorale, Potentiel de membrane mitochondriale.
English descriptors
- KwdEn :
- Acetylcysteine (pharmacology), Antineoplastic Agents (pharmacology), Apoptosis (MeSH), Autophagy (MeSH), Basidiomycota (chemistry), Caspase Inhibitors (pharmacology), Cell Line, Tumor (MeSH), DNA Fragmentation (MeSH), Endodeoxyribonucleases (metabolism), Fungal Polysaccharides (pharmacology), Humans (MeSH), Leukemia, Myeloid (metabolism), Membrane Potential, Mitochondrial (MeSH), Mitochondria (drug effects), Mitochondria (metabolism), Monocytes (drug effects), Monocytes (metabolism), Reactive Oxygen Species (metabolism).
- MESH :
- chemical , metabolism : Endodeoxyribonucleases, Reactive Oxygen Species.
- chemical , pharmacology : Acetylcysteine, Antineoplastic Agents, Caspase Inhibitors, Fungal Polysaccharides.
- chemistry : Basidiomycota.
- drug effects : Mitochondria, Monocytes.
- metabolism : Leukemia, Myeloid, Mitochondria, Monocytes.
- Apoptosis, Autophagy, Cell Line, Tumor, DNA Fragmentation, Humans, Membrane Potential, Mitochondrial.
Abstract
Acute leukemia is one of the commonly diagnosed neoplasms and causes human death. However, the treatment for acute leukemia is not yet satisfactory. Studies have shown that mushroom-derived polysaccharides display low toxicity and have been used clinically for cancer therapy. Therefore, we set out to evaluate the anti-cancerous efficacy of a water-soluble polysaccharide extract from Inonotus taiwanensis (WSPIS) on human acute monocytic leukemia THP-1 and U937 cell lines in vitro. Under our experimental conditions, WSPIS elicited dose-dependent growth retardation and induced apoptotic cell death. Further analysis showed that WSPIS-induced apoptosis was associated with a mitochondrial apoptotic pathway, such as the disruption of mitochondrial membrane potential (MMP), followed by the activation of caspase-9, caspase-3, and PARP (poly(ADP-ribose) polymerase) cleavage. However, a broad caspase inhibitor, Z-VAD.fmk, could not prevent WSPIS-induced apoptosis. These data imply that mechanism(s) other than caspase might be involved. Thus, the involvement of endonuclease G (endoG), a mediator arbitrating caspase-independent oligonucleosomal DNA fragmentation, was examined. Western blotting demonstrated that WSPIS could elicit nuclear translocation of endoG. MMP disruption after WSPIS treatment was accompanied by intracellular reactive oxygen species (ROS) generation. However, pretreatment with N-acetyl-l-cysteine (NAC) could not attenuate WSPIS-induced apoptosis. In addition, our data also show that WSPIS could inhibit autophagy. Activation of autophagy by rapamycin decreased WSPIS-induced apoptosis and cell death. Taken together, our findings suggest that cell cycle arrest, endonuclease G-mediated apoptosis, and autophagy inhibition contribute to the anti-cancerous effect of WSPIS on human acute monocytic leukemia cells.
DOI: 10.3390/ijms19020393
PubMed: 29382173
PubMed Central: PMC5855615
Affiliations:
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xml:lang="en">Anti-Cancerous Effect of Inonotus taiwanensis Polysaccharide Extract on Human Acute Monocytic Leukemia Cells through ROS-Independent Intrinsic Mitochondrial Pathway.</title><author><name sortKey="Chao, Tsai Ling" sort="Chao, Tsai Ling" uniqKey="Chao T" first="Tsai-Ling" last="Chao">Tsai-Ling Chao</name><affiliation wicri:level="1"><nlm:affiliation>Departments of Laboratory Medicine, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung 833, Taiwan. tsaeling@cgmh.org.tw.</nlm:affiliation><country xml:lang="fr">Taïwan</country><wicri:regionArea>Departments of Laboratory Medicine, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung 833</wicri:regionArea><wicri:noRegion>Kaohsiung 833</wicri:noRegion></affiliation><affiliation wicri:level="1"><nlm:affiliation>Department of Medical Laboratory Science and Biotechnology, Fooyin University, Kaohsiung 831, Taiwan. tsaeling@cgmh.org.tw.</nlm:affiliation><country xml:lang="fr">Taïwan</country><wicri:regionArea>Department of Medical Laboratory Science and Biotechnology, Fooyin University, Kaohsiung 831</wicri:regionArea><wicri:noRegion>Kaohsiung 831</wicri:noRegion></affiliation></author><author><name sortKey="Wang, Ting Yin" sort="Wang, Ting Yin" uniqKey="Wang T" first="Ting-Yin" last="Wang">Ting-Yin Wang</name><affiliation wicri:level="1"><nlm:affiliation>Department of Laboratory Medicine, Yunlin Christian Hospital, Yunlin 648, Taiwan. phoebe82825@gmail.com.</nlm:affiliation><country xml:lang="fr">Taïwan</country><wicri:regionArea>Department of Laboratory Medicine, Yunlin Christian Hospital, Yunlin 648</wicri:regionArea><wicri:noRegion>Yunlin 648</wicri:noRegion></affiliation></author><author><name sortKey="Lee, Chin Huei" sort="Lee, Chin Huei" uniqKey="Lee C" first="Chin-Huei" last="Lee">Chin-Huei Lee</name><affiliation wicri:level="1"><nlm:affiliation>Department of Biological Sciences, National Sun Yat-Sen University, Kaohsiung 804, Taiwan. 5MT970038@live.fy.edu.tw.</nlm:affiliation><country xml:lang="fr">Taïwan</country><wicri:regionArea>Department of Biological Sciences, National Sun Yat-Sen University, Kaohsiung 804</wicri:regionArea><wicri:noRegion>Kaohsiung 804</wicri:noRegion></affiliation></author><author><name sortKey="Yiin, Shuenn Jiun" sort="Yiin, Shuenn Jiun" uniqKey="Yiin S" first="Shuenn-Jiun" last="Yiin">Shuenn-Jiun Yiin</name><affiliation wicri:level="1"><nlm:affiliation>Department of Nursing, Tajen University, Pintung 907, Taiwan. yiinsj@tajen.edu.tw.</nlm:affiliation><country xml:lang="fr">Taïwan</country><wicri:regionArea>Department of Nursing, Tajen University, Pintung 907</wicri:regionArea><wicri:noRegion>Pintung 907</wicri:noRegion></affiliation></author><author><name sortKey="Ho, Chun Te" sort="Ho, Chun Te" uniqKey="Ho C" first="Chun-Te" last="Ho">Chun-Te Ho</name><affiliation wicri:level="1"><nlm:affiliation>Graduate Institute of Medical Sciences, College of Medicine, Taipei Medical University, Taipei 110, Taiwan. homenjer@gmail.com.</nlm:affiliation><country xml:lang="fr">Taïwan</country><wicri:regionArea>Graduate Institute of Medical Sciences, College of Medicine, Taipei Medical University, Taipei 110</wicri:regionArea><wicri:noRegion>Taipei 110</wicri:noRegion></affiliation></author><author><name sortKey="Wu, Sheng Hua" sort="Wu, Sheng Hua" uniqKey="Wu S" first="Sheng-Hua" last="Wu">Sheng-Hua Wu</name><affiliation wicri:level="1"><nlm:affiliation>Department of Biology, National Museum of Natural Science, Taichung 404, Taiwan. shwu@mail.nmns.edu.tw.</nlm:affiliation><country xml:lang="fr">Taïwan</country><wicri:regionArea>Department of Biology, National Museum of Natural Science, Taichung 404</wicri:regionArea><wicri:noRegion>Taichung 404</wicri:noRegion></affiliation></author><author><name sortKey="You, Huey Ling" sort="You, Huey Ling" uniqKey="You H" first="Huey-Ling" last="You">Huey-Ling You</name><affiliation wicri:level="1"><nlm:affiliation>Departments of Laboratory Medicine, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung 833, Taiwan. youhling@cgmh.org.tw.</nlm:affiliation><country xml:lang="fr">Taïwan</country><wicri:regionArea>Departments of Laboratory Medicine, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung 833</wicri:regionArea><wicri:noRegion>Kaohsiung 833</wicri:noRegion></affiliation><affiliation wicri:level="1"><nlm:affiliation>Department of Medical Laboratory Science and Biotechnology, Fooyin University, Kaohsiung 831, Taiwan. youhling@cgmh.org.tw.</nlm:affiliation><country xml:lang="fr">Taïwan</country><wicri:regionArea>Department of Medical Laboratory Science and Biotechnology, Fooyin University, Kaohsiung 831</wicri:regionArea><wicri:noRegion>Kaohsiung 831</wicri:noRegion></affiliation></author><author><name sortKey="Chern, Chi Liang" sort="Chern, Chi Liang" uniqKey="Chern C" first="Chi-Liang" last="Chern">Chi-Liang Chern</name><affiliation wicri:level="1"><nlm:affiliation>Department of Medical Laboratory Science and Biotechnology, Fooyin University, Kaohsiung 831, Taiwan. mt115@fy.edu.tw.</nlm:affiliation><country xml:lang="fr">Taïwan</country><wicri:regionArea>Department of Medical Laboratory Science and Biotechnology, Fooyin University, Kaohsiung 831</wicri:regionArea><wicri:noRegion>Kaohsiung 831</wicri:noRegion></affiliation></author></analytic><series><title level="j">International journal of molecular sciences</title><idno type="eISSN">1422-0067</idno><imprint><date when="2018" type="published">2018</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Acetylcysteine (pharmacology)</term><term>Antineoplastic Agents (pharmacology)</term><term>Apoptosis (MeSH)</term><term>Autophagy (MeSH)</term><term>Basidiomycota (chemistry)</term><term>Caspase Inhibitors (pharmacology)</term><term>Cell Line, Tumor (MeSH)</term><term>DNA Fragmentation (MeSH)</term><term>Endodeoxyribonucleases (metabolism)</term><term>Fungal Polysaccharides (pharmacology)</term><term>Humans (MeSH)</term><term>Leukemia, Myeloid (metabolism)</term><term>Membrane Potential, Mitochondrial (MeSH)</term><term>Mitochondria (drug effects)</term><term>Mitochondria (metabolism)</term><term>Monocytes (drug effects)</term><term>Monocytes (metabolism)</term><term>Reactive Oxygen Species (metabolism)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Acétylcystéine (pharmacologie)</term><term>Antinéoplasiques (pharmacologie)</term><term>Apoptose (MeSH)</term><term>Autophagie (MeSH)</term><term>Basidiomycota (composition chimique)</term><term>Endodeoxyribonucleases (métabolisme)</term><term>Espèces réactives de l'oxygène (métabolisme)</term><term>Fragmentation de l'ADN (MeSH)</term><term>Humains (MeSH)</term><term>Inhibiteurs des caspases (pharmacologie)</term><term>Leucémie myéloïde (métabolisme)</term><term>Lignée cellulaire tumorale (MeSH)</term><term>Mitochondries (effets des médicaments et des substances chimiques)</term><term>Mitochondries (métabolisme)</term><term>Monocytes (effets des médicaments et des substances chimiques)</term><term>Monocytes (métabolisme)</term><term>Polysaccharides fongiques (pharmacologie)</term><term>Potentiel de membrane mitochondriale (MeSH)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Endodeoxyribonucleases</term><term>Reactive Oxygen Species</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Acetylcysteine</term><term>Antineoplastic Agents</term><term>Caspase Inhibitors</term><term>Fungal Polysaccharides</term></keywords><keywords scheme="MESH" qualifier="chemistry" xml:lang="en"><term>Basidiomycota</term></keywords><keywords scheme="MESH" qualifier="composition chimique" xml:lang="fr"><term>Basidiomycota</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Mitochondria</term><term>Monocytes</term></keywords><keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Mitochondries</term><term>Monocytes</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Leukemia, Myeloid</term><term>Mitochondria</term><term>Monocytes</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Endodeoxyribonucleases</term><term>Espèces réactives de l'oxygène</term><term>Leucémie myéloïde</term><term>Mitochondries</term><term>Monocytes</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Acétylcystéine</term><term>Antinéoplasiques</term><term>Inhibiteurs des caspases</term><term>Polysaccharides fongiques</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Apoptosis</term><term>Autophagy</term><term>Cell Line, Tumor</term><term>DNA Fragmentation</term><term>Humans</term><term>Membrane Potential, Mitochondrial</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Apoptose</term><term>Autophagie</term><term>Fragmentation de l'ADN</term><term>Humains</term><term>Lignée cellulaire tumorale</term><term>Potentiel de membrane mitochondriale</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Acute leukemia is one of the commonly diagnosed neoplasms and causes human death. However, the treatment for acute leukemia is not yet satisfactory. Studies have shown that mushroom-derived polysaccharides display low toxicity and have been used clinically for cancer therapy. Therefore, we set out to evaluate the anti-cancerous efficacy of a water-soluble polysaccharide extract from <i>Inonotus taiwanensis</i> (WSPIS) on human acute monocytic leukemia THP-1 and U937 cell lines in vitro. Under our experimental conditions, WSPIS elicited dose-dependent growth retardation and induced apoptotic cell death. Further analysis showed that WSPIS-induced apoptosis was associated with a mitochondrial apoptotic pathway, such as the disruption of mitochondrial membrane potential (MMP), followed by the activation of caspase-9, caspase-3, and PARP (poly(ADP-ribose) polymerase) cleavage. However, a broad caspase inhibitor, Z-VAD.fmk, could not prevent WSPIS-induced apoptosis. These data imply that mechanism(s) other than caspase might be involved. Thus, the involvement of endonuclease G (endoG), a mediator arbitrating caspase-independent oligonucleosomal DNA fragmentation, was examined. Western blotting demonstrated that WSPIS could elicit nuclear translocation of endoG. MMP disruption after WSPIS treatment was accompanied by intracellular reactive oxygen species (ROS) generation. However, pretreatment with <i>N</i>-acetyl-l-cysteine (NAC) could not attenuate WSPIS-induced apoptosis. In addition, our data also show that WSPIS could inhibit autophagy. Activation of autophagy by rapamycin decreased WSPIS-induced apoptosis and cell death. Taken together, our findings suggest that cell cycle arrest, endonuclease G-mediated apoptosis, and autophagy inhibition contribute to the anti-cancerous effect of WSPIS on human acute monocytic leukemia cells.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">29382173</PMID><DateCompleted><Year>2018</Year><Month>08</Month><Day>01</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">1422-0067</ISSN><JournalIssue CitedMedium="Internet"><Volume>19</Volume><Issue>2</Issue><PubDate><Year>2018</Year><Month>Jan</Month><Day>29</Day></PubDate></JournalIssue><Title>International journal of molecular sciences</Title><ISOAbbreviation>Int J Mol Sci</ISOAbbreviation></Journal><ArticleTitle>Anti-Cancerous Effect of Inonotus taiwanensis Polysaccharide Extract on Human Acute Monocytic Leukemia Cells through ROS-Independent Intrinsic Mitochondrial Pathway.</ArticleTitle><ELocationID EIdType="pii" ValidYN="Y">E393</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.3390/ijms19020393</ELocationID><Abstract><AbstractText>Acute leukemia is one of the commonly diagnosed neoplasms and causes human death. However, the treatment for acute leukemia is not yet satisfactory. Studies have shown that mushroom-derived polysaccharides display low toxicity and have been used clinically for cancer therapy. Therefore, we set out to evaluate the anti-cancerous efficacy of a water-soluble polysaccharide extract from <i>Inonotus taiwanensis</i> (WSPIS) on human acute monocytic leukemia THP-1 and U937 cell lines in vitro. Under our experimental conditions, WSPIS elicited dose-dependent growth retardation and induced apoptotic cell death. Further analysis showed that WSPIS-induced apoptosis was associated with a mitochondrial apoptotic pathway, such as the disruption of mitochondrial membrane potential (MMP), followed by the activation of caspase-9, caspase-3, and PARP (poly(ADP-ribose) polymerase) cleavage. However, a broad caspase inhibitor, Z-VAD.fmk, could not prevent WSPIS-induced apoptosis. These data imply that mechanism(s) other than caspase might be involved. Thus, the involvement of endonuclease G (endoG), a mediator arbitrating caspase-independent oligonucleosomal DNA fragmentation, was examined. Western blotting demonstrated that WSPIS could elicit nuclear translocation of endoG. MMP disruption after WSPIS treatment was accompanied by intracellular reactive oxygen species (ROS) generation. However, pretreatment with <i>N</i>-acetyl-l-cysteine (NAC) could not attenuate WSPIS-induced apoptosis. In addition, our data also show that WSPIS could inhibit autophagy. Activation of autophagy by rapamycin decreased WSPIS-induced apoptosis and cell death. Taken together, our findings suggest that cell cycle arrest, endonuclease G-mediated apoptosis, and autophagy inhibition contribute to the anti-cancerous effect of WSPIS on human acute monocytic leukemia cells.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Chao</LastName><ForeName>Tsai-Ling</ForeName><Initials>TL</Initials><AffiliationInfo><Affiliation>Departments of Laboratory Medicine, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung 833, Taiwan. tsaeling@cgmh.org.tw.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Medical Laboratory Science and Biotechnology, Fooyin University, Kaohsiung 831, Taiwan. tsaeling@cgmh.org.tw.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Ting-Yin</ForeName><Initials>TY</Initials><AffiliationInfo><Affiliation>Department of Laboratory Medicine, Yunlin Christian Hospital, Yunlin 648, Taiwan. phoebe82825@gmail.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lee</LastName><ForeName>Chin-Huei</ForeName><Initials>CH</Initials><AffiliationInfo><Affiliation>Department of Biological Sciences, National Sun Yat-Sen University, Kaohsiung 804, Taiwan. 5MT970038@live.fy.edu.tw.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yiin</LastName><ForeName>Shuenn-Jiun</ForeName><Initials>SJ</Initials><AffiliationInfo><Affiliation>Department of Nursing, Tajen University, Pintung 907, Taiwan. yiinsj@tajen.edu.tw.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ho</LastName><ForeName>Chun-Te</ForeName><Initials>CT</Initials><AffiliationInfo><Affiliation>Graduate Institute of Medical Sciences, College of Medicine, Taipei Medical University, Taipei 110, Taiwan. homenjer@gmail.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wu</LastName><ForeName>Sheng-Hua</ForeName><Initials>SH</Initials><AffiliationInfo><Affiliation>Department of Biology, National Museum of Natural Science, Taichung 404, Taiwan. shwu@mail.nmns.edu.tw.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>You</LastName><ForeName>Huey-Ling</ForeName><Initials>HL</Initials><AffiliationInfo><Affiliation>Departments of Laboratory Medicine, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung 833, Taiwan. youhling@cgmh.org.tw.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Medical Laboratory Science and Biotechnology, Fooyin University, Kaohsiung 831, Taiwan. youhling@cgmh.org.tw.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chern</LastName><ForeName>Chi-Liang</ForeName><Initials>CL</Initials><AffiliationInfo><Affiliation>Department of Medical Laboratory Science and Biotechnology, Fooyin University, Kaohsiung 831, Taiwan. mt115@fy.edu.tw.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2018</Year><Month>01</Month><Day>29</Day></ArticleDate></Article><MedlineJournalInfo><Country>Switzerland</Country><MedlineTA>Int J Mol Sci</MedlineTA><NlmUniqueID>101092791</NlmUniqueID><ISSNLinking>1422-0067</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000970">Antineoplastic Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D061945">Caspase Inhibitors</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D062610">Fungal Polysaccharides</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D017382">Reactive Oxygen Species</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.1.-</RegistryNumber><NameOfSubstance UI="D004706">Endodeoxyribonucleases</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.1.21.-</RegistryNumber><NameOfSubstance UI="C052391">endonuclease G</NameOfSubstance></Chemical><Chemical><RegistryNumber>WYQ7N0BPYC</RegistryNumber><NameOfSubstance UI="D000111">Acetylcysteine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000111" MajorTopicYN="N">Acetylcysteine</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000970" MajorTopicYN="N">Antineoplastic Agents</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017209" MajorTopicYN="Y">Apoptosis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001343" MajorTopicYN="N">Autophagy</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001487" MajorTopicYN="N">Basidiomycota</DescriptorName><QualifierName UI="Q000737" MajorTopicYN="Y">chemistry</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D061945" MajorTopicYN="N">Caspase Inhibitors</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</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="D004706" MajorTopicYN="N">Endodeoxyribonucleases</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D062610" MajorTopicYN="N">Fungal Polysaccharides</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007951" MajorTopicYN="N">Leukemia, Myeloid</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D053078" MajorTopicYN="N">Membrane Potential, Mitochondrial</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008928" MajorTopicYN="N">Mitochondria</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009000" MajorTopicYN="N">Monocytes</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017382" MajorTopicYN="N">Reactive Oxygen Species</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Inonotus taiwanensis</Keyword><Keyword MajorTopicYN="N">apoptosis</Keyword><Keyword MajorTopicYN="N">endonuclease G</Keyword><Keyword MajorTopicYN="N">human acute monocytic leukemia cell line</Keyword></KeywordList><CoiStatement>The authors declare no conflict of interest.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2017</Year><Month>11</Month><Day>13</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2018</Year><Month>01</Month><Day>03</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2018</Year><Month>01</Month><Day>19</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2018</Year><Month>2</Month><Day>1</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2018</Year><Month>2</Month><Day>1</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2018</Year><Month>8</Month><Day>2</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">29382173</ArticleId><ArticleId IdType="pii">ijms19020393</ArticleId><ArticleId IdType="doi">10.3390/ijms19020393</ArticleId><ArticleId IdType="pmc">PMC5855615</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Cancer Manag Res. 2012;4:357-65</Citation><ArticleIdList><ArticleId IdType="pubmed">23091399</ArticleId></ArticleIdList></Reference><Reference><Citation>Anal Biochem. 2005 Apr 1;339(1):69-72</Citation><ArticleIdList><ArticleId IdType="pubmed">15766712</ArticleId></ArticleIdList></Reference><Reference><Citation>Nature. 1969 May 17;222(5194):687-8</Citation><ArticleIdList><ArticleId 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name="Taïwan"><noRegion><name sortKey="Chao, Tsai Ling" sort="Chao, Tsai Ling" uniqKey="Chao T" first="Tsai-Ling" last="Chao">Tsai-Ling Chao</name></noRegion><name sortKey="Chao, Tsai Ling" sort="Chao, Tsai Ling" uniqKey="Chao T" first="Tsai-Ling" last="Chao">Tsai-Ling Chao</name><name sortKey="Chern, Chi Liang" sort="Chern, Chi Liang" uniqKey="Chern C" first="Chi-Liang" last="Chern">Chi-Liang Chern</name><name sortKey="Ho, Chun Te" sort="Ho, Chun Te" uniqKey="Ho C" first="Chun-Te" last="Ho">Chun-Te Ho</name><name sortKey="Lee, Chin Huei" sort="Lee, Chin Huei" uniqKey="Lee C" first="Chin-Huei" last="Lee">Chin-Huei Lee</name><name sortKey="Wang, Ting Yin" sort="Wang, Ting Yin" uniqKey="Wang T" first="Ting-Yin" last="Wang">Ting-Yin Wang</name><name sortKey="Wu, Sheng Hua" sort="Wu, Sheng Hua" uniqKey="Wu S" first="Sheng-Hua" last="Wu">Sheng-Hua Wu</name><name sortKey="Yiin, Shuenn Jiun" sort="Yiin, Shuenn Jiun" uniqKey="Yiin S" first="Shuenn-Jiun" last="Yiin">Shuenn-Jiun Yiin</name><name sortKey="You, Huey Ling" sort="You, Huey Ling" uniqKey="You H" first="Huey-Ling" last="You">Huey-Ling You</name><name sortKey="You, Huey Ling" sort="You, Huey Ling" uniqKey="You H" first="Huey-Ling" last="You">Huey-Ling You</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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