4-Acetylantrocamol LT3, a New Ubiquinone from Antrodia cinnamomea, Inhibits Hepatocellular Carcinoma HepG2 Cell Growth by Targeting YAP/TAZ, mTOR, and WNT/β-Catenin Signaling.
Identifieur interne : 000163 ( Main/Exploration ); précédent : 000162; suivant : 0001644-Acetylantrocamol LT3, a New Ubiquinone from Antrodia cinnamomea, Inhibits Hepatocellular Carcinoma HepG2 Cell Growth by Targeting YAP/TAZ, mTOR, and WNT/β-Catenin Signaling.
Auteurs : Yen-Lin Chen [Taïwan] ; I-Chuan Yen [Taïwan] ; Kuen-Tze Lin [Taïwan] ; Feng-Yi Lai [Taïwan] ; Shih-Yu Lee [Taïwan]Source :
- The American journal of Chinese medicine [ 1793-6853 ] ; 2020.
Descripteurs français
- KwdFr :
- Antinéoplasiques d'origine végétale (MeSH), Antrodia (composition chimique), Autophagie (effets des médicaments et des substances chimiques), Autophagie (génétique), Carcinome hépatocellulaire (anatomopathologie), Carcinome hépatocellulaire (génétique), Cellules HepG2 (MeSH), Facteurs de transcription (métabolisme), Humains (MeSH), Protéines adaptatrices de la transduction du signal (métabolisme), Protéines de type Wingless (métabolisme), Sérine-thréonine kinases TOR (métabolisme), Transduction du signal (effets des médicaments et des substances chimiques), Tumeurs du foie (anatomopathologie), Tumeurs du foie (génétique), Ubiquinones (analogues et dérivés), Ubiquinones (isolement et purification), Ubiquinones (pharmacologie), bêta-Caténine (métabolisme).
- MESH :
- analogues et dérivés : Ubiquinones.
- anatomopathologie : Carcinome hépatocellulaire, Tumeurs du foie.
- composition chimique : Antrodia.
- effets des médicaments et des substances chimiques : Autophagie, Transduction du signal.
- génétique : Autophagie, Carcinome hépatocellulaire, Tumeurs du foie.
- isolement et purification : Ubiquinones.
- métabolisme : Facteurs de transcription, Protéines adaptatrices de la transduction du signal, Protéines de type Wingless, Sérine-thréonine kinases TOR, bêta-Caténine.
- pharmacologie : Ubiquinones.
- Antinéoplasiques d'origine végétale, Cellules HepG2, Humains.
English descriptors
- KwdEn :
- Adaptor Proteins, Signal Transducing (metabolism), Antineoplastic Agents, Phytogenic (MeSH), Antrodia (chemistry), Autophagy (drug effects), Autophagy (genetics), Carcinoma, Hepatocellular (genetics), Carcinoma, Hepatocellular (pathology), Hep G2 Cells (MeSH), Humans (MeSH), Liver Neoplasms (genetics), Liver Neoplasms (pathology), Signal Transduction (drug effects), TOR Serine-Threonine Kinases (metabolism), Transcription Factors (metabolism), Ubiquinone (analogs & derivatives), Ubiquinone (isolation & purification), Ubiquinone (pharmacology), Wnt Proteins (metabolism), beta Catenin (metabolism).
- MESH :
- chemical , analogs & derivatives : Ubiquinone.
- chemical , isolation & purification : Ubiquinone.
- chemical , metabolism : Adaptor Proteins, Signal Transducing, TOR Serine-Threonine Kinases, Transcription Factors, Wnt Proteins, beta Catenin.
- chemical , pharmacology : Ubiquinone.
- chemical : Antineoplastic Agents, Phytogenic.
- chemistry : Antrodia.
- drug effects : Autophagy, Signal Transduction.
- genetics : Autophagy, Carcinoma, Hepatocellular, Liver Neoplasms.
- pathology : Carcinoma, Hepatocellular, Liver Neoplasms.
- Hep G2 Cells, Humans.
Abstract
4-acetylantrocamol LT3 (4AALT3), a new ubiquinone from the mycelium of Antrodia cinnamomea (Polyporaceae), has been recently shown to possess anticancer activity. However, the detailed mechanisms of such action remain unclear. In this study, the molecular mechanisms of 4AALT3 on hepatocellular carcinoma cells (HCC) were investigated. Human hepatocellular carcinoma cell line HepG2 cells were treated with concentrations of 4AALT3. Cell viability, colony formation, and the underlying mechanisms were then analyzed by CCK-8, colony formation, qPCR, and Western blotting assays. We found that 4AALT3 significantly decreased cell viability and colony formation in a dose-dependent manner. Accordingly, 4AALT3 significantly decreased protein levels of cyclin B, E1, D1, and D3, thereby facilitating cell cycle arrest. In addition, 4AALT3 significantly suppressed the nuclear localization of Yes-associated protein (YAP)/transcriptional co-activator with PDZ-binding motif (TAZ), mammalian target of rapamycin (mTOR), and WNT/[Formula: see text]-catenin signaling pathways, all of which are well-known signaling pathways that contribute to the malignant properties of HCC. These effects are associated with activation of 5' AMP-activated protein kinase (AMPK) and autophagy. Our findings indicate that 4AALT3 exerts inhibitory effects on HepG2 cell growth via multiple signaling pathways and may be a potential agent for HCC therapy.
DOI: 10.1142/S0192415X20500615
PubMed: 32668963
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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National Defense Medical Center, Taipei, Taiwan.</nlm:affiliation><country xml:lang="fr">Taïwan</country><wicri:regionArea>Graduate Institute of Medical Sciences, National Defense Medical Center, Taipei</wicri:regionArea><wicri:noRegion>Taipei</wicri:noRegion></affiliation><affiliation wicri:level="1"><nlm:affiliation>Department of Radiology, Taoyuan Armed Forces General Hospital, National Defense Medical Center, Taipei, Taiwan.</nlm:affiliation><country xml:lang="fr">Taïwan</country><wicri:regionArea>Department of Radiology, Taoyuan Armed Forces General Hospital, National Defense Medical Center, Taipei</wicri:regionArea><wicri:noRegion>Taipei</wicri:noRegion></affiliation></author><author><name sortKey="Yen, I Chuan" sort="Yen, I Chuan" uniqKey="Yen I" first="I-Chuan" last="Yen">I-Chuan Yen</name><affiliation wicri:level="1"><nlm:affiliation>School of Pharmacy, National Defense Medical Center, Taipei, Taiwan.</nlm:affiliation><country xml:lang="fr">Taïwan</country><wicri:regionArea>School of Pharmacy, National Defense Medical Center, Taipei</wicri:regionArea><wicri:noRegion>Taipei</wicri:noRegion></affiliation></author><author><name sortKey="Lin, Kuen Tze" sort="Lin, Kuen Tze" uniqKey="Lin K" first="Kuen-Tze" last="Lin">Kuen-Tze Lin</name><affiliation wicri:level="1"><nlm:affiliation>Graduate Institute of Medical Sciences, National Defense Medical Center, Taipei, Taiwan.</nlm:affiliation><country xml:lang="fr">Taïwan</country><wicri:regionArea>Graduate Institute of Medical Sciences, National Defense Medical Center, Taipei</wicri:regionArea><wicri:noRegion>Taipei</wicri:noRegion></affiliation><affiliation wicri:level="1"><nlm:affiliation>Department of Radiation Oncology, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan.</nlm:affiliation><country xml:lang="fr">Taïwan</country><wicri:regionArea>Department of Radiation Oncology, Tri-Service General Hospital, National Defense Medical Center, 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(genetics)</term><term>Carcinoma, Hepatocellular (genetics)</term><term>Carcinoma, Hepatocellular (pathology)</term><term>Hep G2 Cells (MeSH)</term><term>Humans (MeSH)</term><term>Liver Neoplasms (genetics)</term><term>Liver Neoplasms (pathology)</term><term>Signal Transduction (drug effects)</term><term>TOR Serine-Threonine Kinases (metabolism)</term><term>Transcription Factors (metabolism)</term><term>Ubiquinone (analogs & derivatives)</term><term>Ubiquinone (isolation & purification)</term><term>Ubiquinone (pharmacology)</term><term>Wnt Proteins (metabolism)</term><term>beta Catenin (metabolism)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Antinéoplasiques d'origine végétale (MeSH)</term><term>Antrodia (composition chimique)</term><term>Autophagie (effets des médicaments et des substances chimiques)</term><term>Autophagie (génétique)</term><term>Carcinome hépatocellulaire (anatomopathologie)</term><term>Carcinome hépatocellulaire (génétique)</term><term>Cellules HepG2 (MeSH)</term><term>Facteurs de transcription (métabolisme)</term><term>Humains (MeSH)</term><term>Protéines adaptatrices de la transduction du signal (métabolisme)</term><term>Protéines de type Wingless (métabolisme)</term><term>Sérine-thréonine kinases TOR (métabolisme)</term><term>Transduction du signal (effets des médicaments et des substances chimiques)</term><term>Tumeurs du foie (anatomopathologie)</term><term>Tumeurs du foie (génétique)</term><term>Ubiquinones (analogues et dérivés)</term><term>Ubiquinones (isolement et purification)</term><term>Ubiquinones (pharmacologie)</term><term>bêta-Caténine (métabolisme)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analogs & derivatives" xml:lang="en"><term>Ubiquinone</term></keywords><keywords scheme="MESH" type="chemical" qualifier="isolation & purification" xml:lang="en"><term>Ubiquinone</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Adaptor Proteins, Signal Transducing</term><term>TOR Serine-Threonine Kinases</term><term>Transcription Factors</term><term>Wnt Proteins</term><term>beta Catenin</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Ubiquinone</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>Antineoplastic Agents, Phytogenic</term></keywords><keywords scheme="MESH" qualifier="analogues et dérivés" xml:lang="fr"><term>Ubiquinones</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Carcinome hépatocellulaire</term><term>Tumeurs du foie</term></keywords><keywords scheme="MESH" qualifier="chemistry" xml:lang="en"><term>Antrodia</term></keywords><keywords scheme="MESH" qualifier="composition chimique" xml:lang="fr"><term>Antrodia</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Autophagy</term><term>Signal Transduction</term></keywords><keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Autophagie</term><term>Transduction du signal</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Autophagy</term><term>Carcinoma, Hepatocellular</term><term>Liver Neoplasms</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Autophagie</term><term>Carcinome hépatocellulaire</term><term>Tumeurs du foie</term></keywords><keywords scheme="MESH" qualifier="isolement et purification" xml:lang="fr"><term>Ubiquinones</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Facteurs de transcription</term><term>Protéines adaptatrices de la transduction du signal</term><term>Protéines de type Wingless</term><term>Sérine-thréonine kinases TOR</term><term>bêta-Caténine</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Carcinoma, Hepatocellular</term><term>Liver Neoplasms</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Ubiquinones</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Hep G2 Cells</term><term>Humans</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Antinéoplasiques d'origine végétale</term><term>Cellules HepG2</term><term>Humains</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">4-acetylantrocamol LT3 (4AALT3), a new ubiquinone from the mycelium of <i>Antrodia cinnamomea</i> (Polyporaceae), has been recently shown to possess anticancer activity. However, the detailed mechanisms of such action remain unclear. In this study, the molecular mechanisms of 4AALT3 on hepatocellular carcinoma cells (HCC) were investigated. Human hepatocellular carcinoma cell line HepG2 cells were treated with concentrations of 4AALT3. Cell viability, colony formation, and the underlying mechanisms were then analyzed by CCK-8, colony formation, qPCR, and Western blotting assays. We found that 4AALT3 significantly decreased cell viability and colony formation in a dose-dependent manner. Accordingly, 4AALT3 significantly decreased protein levels of cyclin B, E1, D1, and D3, thereby facilitating cell cycle arrest. In addition, 4AALT3 significantly suppressed the nuclear localization of Yes-associated protein (YAP)/transcriptional co-activator with PDZ-binding motif (TAZ), mammalian target of rapamycin (mTOR), and WNT/[Formula: see text]-catenin signaling pathways, all of which are well-known signaling pathways that contribute to the malignant properties of HCC. These effects are associated with activation of 5' AMP-activated protein kinase (AMPK) and autophagy. Our findings indicate that 4AALT3 exerts inhibitory effects on HepG2 cell growth via multiple signaling pathways and may be a potential agent for HCC therapy.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">32668963</PMID><DateCompleted><Year>2020</Year><Month>10</Month><Day>20</Day></DateCompleted><DateRevised><Year>2020</Year><Month>10</Month><Day>20</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1793-6853</ISSN><JournalIssue CitedMedium="Internet"><Volume>48</Volume><Issue>5</Issue><PubDate><Year>2020</Year></PubDate></JournalIssue><Title>The American journal of Chinese medicine</Title><ISOAbbreviation>Am J Chin Med</ISOAbbreviation></Journal><ArticleTitle>4-Acetylantrocamol LT3, a New Ubiquinone from <i>Antrodia cinnamomea</i>, Inhibits Hepatocellular Carcinoma HepG2 Cell Growth by Targeting YAP/TAZ, mTOR, and WNT/β-Catenin Signaling.</ArticleTitle><Pagination><MedlinePgn>1243-1261</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1142/S0192415X20500615</ELocationID><Abstract><AbstractText>4-acetylantrocamol LT3 (4AALT3), a new ubiquinone from the mycelium of <i>Antrodia cinnamomea</i> (Polyporaceae), has been recently shown to possess anticancer activity. However, the detailed mechanisms of such action remain unclear. In this study, the molecular mechanisms of 4AALT3 on hepatocellular carcinoma cells (HCC) were investigated. Human hepatocellular carcinoma cell line HepG2 cells were treated with concentrations of 4AALT3. Cell viability, colony formation, and the underlying mechanisms were then analyzed by CCK-8, colony formation, qPCR, and Western blotting assays. We found that 4AALT3 significantly decreased cell viability and colony formation in a dose-dependent manner. Accordingly, 4AALT3 significantly decreased protein levels of cyclin B, E1, D1, and D3, thereby facilitating cell cycle arrest. In addition, 4AALT3 significantly suppressed the nuclear localization of Yes-associated protein (YAP)/transcriptional co-activator with PDZ-binding motif (TAZ), mammalian target of rapamycin (mTOR), and WNT/[Formula: see text]-catenin signaling pathways, all of which are well-known signaling pathways that contribute to the malignant properties of HCC. These effects are associated with activation of 5' AMP-activated protein kinase (AMPK) and autophagy. Our findings indicate that 4AALT3 exerts inhibitory effects on HepG2 cell growth via multiple signaling pathways and may be a potential agent for HCC therapy.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Chen</LastName><ForeName>Yen-Lin</ForeName><Initials>YL</Initials><AffiliationInfo><Affiliation>Graduate Institute of Medical Sciences, National Defense Medical Center, Taipei, Taiwan.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Radiology, Taoyuan Armed Forces General Hospital, National Defense Medical Center, Taipei, Taiwan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yen</LastName><ForeName>I-Chuan</ForeName><Initials>IC</Initials><AffiliationInfo><Affiliation>School of Pharmacy, National Defense Medical Center, Taipei, Taiwan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lin</LastName><ForeName>Kuen-Tze</ForeName><Initials>KT</Initials><AffiliationInfo><Affiliation>Graduate Institute of Medical Sciences, National Defense Medical Center, Taipei, Taiwan.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Radiation Oncology, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lai</LastName><ForeName>Feng-Yi</ForeName><Initials>FY</Initials><AffiliationInfo><Affiliation>Graduate Institute of Aerospace and Undersea Medicine, National Defense Medical Center, Taipei, Taiwan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lee</LastName><ForeName>Shih-Yu</ForeName><Initials>SY</Initials><AffiliationInfo><Affiliation>Graduate Institute of Medical Sciences, National Defense Medical Center, Taipei, Taiwan.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Graduate Institute of Aerospace and Undersea Medicine, National Defense Medical Center, Taipei, Taiwan.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>Singapore</Country><MedlineTA>Am J Chin Med</MedlineTA><NlmUniqueID>7901431</NlmUniqueID><ISSNLinking>0192-415X</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D048868">Adaptor Proteins, Signal Transducing</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000972">Antineoplastic Agents, Phytogenic</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C108675">TAZ protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D014157">Transcription Factors</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D051153">Wnt Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C088374">YAP1 (Yes-associated) protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C000598389">antrocamol</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D051176">beta Catenin</NameOfSubstance></Chemical><Chemical><RegistryNumber>1339-63-5</RegistryNumber><NameOfSubstance UI="D014451">Ubiquinone</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.1.1</RegistryNumber><NameOfSubstance UI="C546842">MTOR protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.1.1</RegistryNumber><NameOfSubstance UI="D058570">TOR Serine-Threonine Kinases</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D048868" MajorTopicYN="N">Adaptor Proteins, Signal Transducing</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000972" MajorTopicYN="N">Antineoplastic Agents, Phytogenic</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D055491" MajorTopicYN="N">Antrodia</DescriptorName><QualifierName UI="Q000737" MajorTopicYN="Y">chemistry</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001343" MajorTopicYN="N">Autophagy</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006528" MajorTopicYN="N">Carcinoma, Hepatocellular</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D056945" MajorTopicYN="N">Hep G2 Cells</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008113" MajorTopicYN="N">Liver Neoplasms</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D058570" MajorTopicYN="N">TOR Serine-Threonine Kinases</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014157" MajorTopicYN="N">Transcription Factors</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014451" MajorTopicYN="N">Ubiquinone</DescriptorName><QualifierName UI="Q000031" MajorTopicYN="Y">analogs & derivatives</QualifierName><QualifierName UI="Q000302" MajorTopicYN="N">isolation & purification</QualifierName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051153" MajorTopicYN="N">Wnt Proteins</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051176" MajorTopicYN="N">beta Catenin</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">4-Acetylantrocamol LT3</Keyword><Keyword MajorTopicYN="N">Autophagy</Keyword><Keyword MajorTopicYN="N">Hepatocellular Carcinoma Cells</Keyword><Keyword MajorTopicYN="N">Wnt/[Formula: see text]-Catenin, mTOR</Keyword><Keyword MajorTopicYN="N">YAP/TAZ</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2020</Year><Month>7</Month><Day>17</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2020</Year><Month>7</Month><Day>17</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2020</Year><Month>10</Month><Day>21</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">32668963</ArticleId><ArticleId IdType="doi">10.1142/S0192415X20500615</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Taïwan</li></country></list><tree><country name="Taïwan"><noRegion><name sortKey="Chen, Yen Lin" sort="Chen, Yen Lin" uniqKey="Chen Y" first="Yen-Lin" last="Chen">Yen-Lin Chen</name></noRegion><name sortKey="Chen, Yen Lin" sort="Chen, Yen Lin" uniqKey="Chen Y" first="Yen-Lin" last="Chen">Yen-Lin Chen</name><name sortKey="Lai, Feng Yi" sort="Lai, Feng Yi" uniqKey="Lai F" first="Feng-Yi" last="Lai">Feng-Yi Lai</name><name sortKey="Lee, Shih Yu" sort="Lee, Shih Yu" uniqKey="Lee S" first="Shih-Yu" last="Lee">Shih-Yu Lee</name><name sortKey="Lee, Shih Yu" sort="Lee, Shih Yu" uniqKey="Lee S" first="Shih-Yu" last="Lee">Shih-Yu Lee</name><name sortKey="Lin, Kuen Tze" sort="Lin, Kuen Tze" uniqKey="Lin K" first="Kuen-Tze" last="Lin">Kuen-Tze Lin</name><name sortKey="Lin, Kuen Tze" sort="Lin, Kuen Tze" uniqKey="Lin K" first="Kuen-Tze" last="Lin">Kuen-Tze Lin</name><name sortKey="Yen, I Chuan" sort="Yen, I Chuan" uniqKey="Yen I" first="I-Chuan" last="Yen">I-Chuan Yen</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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|texte= 4-Acetylantrocamol LT3, a New Ubiquinone from Antrodia cinnamomea, Inhibits Hepatocellular Carcinoma HepG2 Cell Growth by Targeting YAP/TAZ, mTOR, and WNT/β-Catenin Signaling.
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