RapamycinFungusV1, Main, Exploration, bibRecord, 000487

Suppression of Cell Growth, Migration and Drug Resistance by Ethanolic Extract of Antrodia cinnamomea in Human Lung Cancer A549 Cells and C57BL/6J Allograft Tumor Model.

Identifieur interne : 000487 ( Main/Exploration ); précédent : 000486; suivant : 000488

Suppression of Cell Growth, Migration and Drug Resistance by Ethanolic Extract of Antrodia cinnamomea in Human Lung Cancer A549 Cells and C57BL/6J Allograft Tumor Model.

Auteurs : Chi-Han Wu [Taïwan] ; Fon-Chang Liu [Taïwan] ; Chun-Hsu Pan [Taïwan] ; Ming-Tsung Lai [Taïwan] ; Shou-Jen Lan [Taïwan] ; Chieh-Hsi Wu [Taïwan] ; Ming-Jyh Sheu [Taïwan]

Source :

International journal of molecular sciences [ 1422-0067 ] ; 2018.

RBID : pubmed:29522490

Descripteurs français

KwdFr :
- Allogreffes (MeSH), Animaux (MeSH), Antinéoplasiques (composition chimique), Antinéoplasiques (pharmacologie), Antrodia (composition chimique), Cellules A549 (MeSH), Corps fructifères de champignon (composition chimique), Humains (MeSH), Modèles animaux de maladie humaine (MeSH), Mouvement cellulaire (effets des médicaments et des substances chimiques), Prolifération cellulaire (effets des médicaments et des substances chimiques), Résistance aux médicaments antinéoplasiques (effets des médicaments et des substances chimiques), Souris (MeSH), Souris de lignée C57BL (MeSH), Tumeurs du poumon (traitement médicamenteux), Éthanol (composition chimique).
MESH :
- composition chimique : Antinéoplasiques, Antrodia, Corps fructifères de champignon, Éthanol.
- effets des médicaments et des substances chimiques : Mouvement cellulaire, Prolifération cellulaire, Résistance aux médicaments antinéoplasiques.
- pharmacologie : Antinéoplasiques.
- traitement médicamenteux : Tumeurs du poumon.
- Allogreffes, Animaux, Cellules A549, Humains, Modèles animaux de maladie humaine, Souris, Souris de lignée C57BL.

English descriptors

KwdEn :
- A549 Cells (MeSH), Allografts (MeSH), Animals (MeSH), Antineoplastic Agents (chemistry), Antineoplastic Agents (pharmacology), Antrodia (chemistry), Cell Movement (drug effects), Cell Proliferation (drug effects), Disease Models, Animal (MeSH), Drug Resistance, Neoplasm (drug effects), Ethanol (chemistry), Fruiting Bodies, Fungal (chemistry), Humans (MeSH), Lung Neoplasms (drug therapy), Mice (MeSH), Mice, Inbred C57BL (MeSH).
MESH :
- chemical , chemistry : Antineoplastic Agents, Ethanol.
- chemical , pharmacology : Antineoplastic Agents.
- chemistry : Antrodia, Fruiting Bodies, Fungal.
- drug effects : Cell Movement, Cell Proliferation, Drug Resistance, Neoplasm.
- drug therapy : Lung Neoplasms.
- A549 Cells, Allografts, Animals, Disease Models, Animal, Humans, Mice, Mice, Inbred C57BL.

Abstract

The purpose of this study was to investigate the inhibitory activities of ethanolic extracts from Antrodia cinnamomea (EEAC) on lung cancer. Cell proliferation and cell cycle distribution were analyzed using (3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) (MTT) assay and flow cytometry, respectively. Wound-healing assay, Western blotting, and a murine tumor model were separately used to examine cell migration, protein expression, and tumor repression. Our results showed that EEAC induced cell cycle arrest at the G0/G1 phase resulting decreased cell viability in A549 cells. Moreover, EEAC up-regulated the growth-suppressing proteins, adenosine 5'-monophosphate-activated protein kinase (AMPK), p21 and p27, but down-regulated the growth-promoting proteins, protein kinase B (Akt), mammalian tarfet of rapamycin (mTOR), extracellular signal-regulating kinase 1/2 (ERK1/2), retinoblastoma protein (Rb), cyclin E, and cyclin D1. EEAC also inhibited A549 cell migration and reduced expression of gelatinases. In addition, our data showed that tumor growth was suppressed after treatment with EEAC in a murine allograft tumor model. Some bioactive compounds from EEAC, such as cordycepin and zhankuic acid A, were demonstrated to reduce the protein expressions of matrix metalloproteinase (MMP)-9 and cyclin D1 in A549 cells. Furthermore, EEAC enhanced chemosensitivity of A549 to paclitaxel by reducing the protein levels of caveolin-1. Our data suggests that EEAC has the potential to be an adjuvant medicine for the treatment of lung cancer.

DOI: 10.3390/ijms19030791
PubMed: 29522490
PubMed Central: PMC5877652

Affiliations:

Taïwan

Links toward previous steps (curation, corpus...)

to stream Main, to step Corpus: 000601
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Le document en format XML

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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>A549 Cells (MeSH)</term>
<term>Allografts (MeSH)</term>
<term>Animals (MeSH)</term>
<term>Antineoplastic Agents (chemistry)</term>
<term>Antineoplastic Agents (pharmacology)</term>
<term>Antrodia (chemistry)</term>
<term>Cell Movement (drug effects)</term>
<term>Cell Proliferation (drug effects)</term>
<term>Disease Models, Animal (MeSH)</term>
<term>Drug Resistance, Neoplasm (drug effects)</term>
<term>Ethanol (chemistry)</term>
<term>Fruiting Bodies, Fungal (chemistry)</term>
<term>Humans (MeSH)</term>
<term>Lung Neoplasms (drug therapy)</term>
<term>Mice (MeSH)</term>
<term>Mice, Inbred C57BL (MeSH)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Allogreffes (MeSH)</term>
<term>Animaux (MeSH)</term>
<term>Antinéoplasiques (composition chimique)</term>
<term>Antinéoplasiques (pharmacologie)</term>
<term>Antrodia (composition chimique)</term>
<term>Cellules A549 (MeSH)</term>
<term>Corps fructifères de champignon (composition chimique)</term>
<term>Humains (MeSH)</term>
<term>Modèles animaux de maladie humaine (MeSH)</term>
<term>Mouvement cellulaire (effets des médicaments et des substances chimiques)</term>
<term>Prolifération cellulaire (effets des médicaments et des substances chimiques)</term>
<term>Résistance aux médicaments antinéoplasiques (effets des médicaments et des substances chimiques)</term>
<term>Souris (MeSH)</term>
<term>Souris de lignée C57BL (MeSH)</term>
<term>Tumeurs du poumon (traitement médicamenteux)</term>
<term>Éthanol (composition chimique)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="chemistry" xml:lang="en"><term>Antineoplastic Agents</term>
<term>Ethanol</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Antineoplastic Agents</term>
</keywords>
<keywords scheme="MESH" qualifier="chemistry" xml:lang="en"><term>Antrodia</term>
<term>Fruiting Bodies, Fungal</term>
</keywords>
<keywords scheme="MESH" qualifier="composition chimique" xml:lang="fr"><term>Antinéoplasiques</term>
<term>Antrodia</term>
<term>Corps fructifères de champignon</term>
<term>Éthanol</term>
</keywords>
<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Cell Movement</term>
<term>Cell Proliferation</term>
<term>Drug Resistance, Neoplasm</term>
</keywords>
<keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Lung Neoplasms</term>
</keywords>
<keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Mouvement cellulaire</term>
<term>Prolifération cellulaire</term>
<term>Résistance aux médicaments antinéoplasiques</term>
</keywords>
<keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Antinéoplasiques</term>
</keywords>
<keywords scheme="MESH" qualifier="traitement médicamenteux" xml:lang="fr"><term>Tumeurs du poumon</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>A549 Cells</term>
<term>Allografts</term>
<term>Animals</term>
<term>Disease Models, Animal</term>
<term>Humans</term>
<term>Mice</term>
<term>Mice, Inbred C57BL</term>
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<term>Animaux</term>
<term>Cellules A549</term>
<term>Humains</term>
<term>Modèles animaux de maladie humaine</term>
<term>Souris</term>
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<front><div type="abstract" xml:lang="en">The purpose of this study was to investigate the inhibitory activities of ethanolic extracts from <i>Antrodia cinnamomea</i>
 (EEAC) on lung cancer. Cell proliferation and cell cycle distribution were analyzed using (3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) (MTT) assay and flow cytometry, respectively. Wound-healing assay, Western blotting, and a murine tumor model were separately used to examine cell migration, protein expression, and tumor repression. Our results showed that EEAC induced cell cycle arrest at the G0/G1 phase resulting decreased cell viability in A549 cells. Moreover, EEAC up-regulated the growth-suppressing proteins, adenosine 5'-monophosphate-activated protein kinase (AMPK), p21 and p27, but down-regulated the growth-promoting proteins, protein kinase B (Akt), mammalian tarfet of rapamycin (mTOR), extracellular signal-regulating kinase 1/2 (ERK1/2), retinoblastoma protein (Rb), cyclin E, and cyclin D1. EEAC also inhibited A549 cell migration and reduced expression of gelatinases. In addition, our data showed that tumor growth was suppressed after treatment with EEAC in a murine allograft tumor model. Some bioactive compounds from EEAC, such as cordycepin and zhankuic acid A, were demonstrated to reduce the protein expressions of matrix metalloproteinase (MMP)-9 and cyclin D1 in A549 cells. Furthermore, EEAC enhanced chemosensitivity of A549 to paclitaxel by reducing the protein levels of caveolin-1. Our data suggests that EEAC has the potential to be an adjuvant medicine for the treatment of lung cancer.</div>
</front>
</TEI>
<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">29522490</PMID>
<DateCompleted><Year>2018</Year>
<Month>09</Month>
<Day>18</Day>
</DateCompleted>
<DateRevised><Year>2018</Year>
<Month>11</Month>
<Day>14</Day>
</DateRevised>
<Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">1422-0067</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>19</Volume>
<Issue>3</Issue>
<PubDate><Year>2018</Year>
<Month>Mar</Month>
<Day>09</Day>
</PubDate>
</JournalIssue>
<Title>International journal of molecular sciences</Title>
<ISOAbbreviation>Int J Mol Sci</ISOAbbreviation>
</Journal>
<ArticleTitle>Suppression of Cell Growth, Migration and Drug Resistance by Ethanolic Extract of Antrodia cinnamomea in Human Lung Cancer A549 Cells and C57BL/6J Allograft Tumor Model.</ArticleTitle>
<ELocationID EIdType="pii" ValidYN="Y">E791</ELocationID>
<ELocationID EIdType="doi" ValidYN="Y">10.3390/ijms19030791</ELocationID>
<Abstract><AbstractText>The purpose of this study was to investigate the inhibitory activities of ethanolic extracts from <i>Antrodia cinnamomea</i>
 (EEAC) on lung cancer. Cell proliferation and cell cycle distribution were analyzed using (3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) (MTT) assay and flow cytometry, respectively. Wound-healing assay, Western blotting, and a murine tumor model were separately used to examine cell migration, protein expression, and tumor repression. Our results showed that EEAC induced cell cycle arrest at the G0/G1 phase resulting decreased cell viability in A549 cells. Moreover, EEAC up-regulated the growth-suppressing proteins, adenosine 5'-monophosphate-activated protein kinase (AMPK), p21 and p27, but down-regulated the growth-promoting proteins, protein kinase B (Akt), mammalian tarfet of rapamycin (mTOR), extracellular signal-regulating kinase 1/2 (ERK1/2), retinoblastoma protein (Rb), cyclin E, and cyclin D1. EEAC also inhibited A549 cell migration and reduced expression of gelatinases. In addition, our data showed that tumor growth was suppressed after treatment with EEAC in a murine allograft tumor model. Some bioactive compounds from EEAC, such as cordycepin and zhankuic acid A, were demonstrated to reduce the protein expressions of matrix metalloproteinase (MMP)-9 and cyclin D1 in A549 cells. Furthermore, EEAC enhanced chemosensitivity of A549 to paclitaxel by reducing the protein levels of caveolin-1. Our data suggests that EEAC has the potential to be an adjuvant medicine for the treatment of lung cancer.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Wu</LastName>
<ForeName>Chi-Han</ForeName>
<Initials>CH</Initials>
<AffiliationInfo><Affiliation>School of Pharmacy, China Medical University, Taichung 40402, Taiwan. u101055003@cmu.edu.tw.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Liu</LastName>
<ForeName>Fon-Chang</ForeName>
<Initials>FC</Initials>
<AffiliationInfo><Affiliation>School of Pharmacy, China Medical University, Taichung 40402, Taiwan. fonchang008@gmail.com.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Pan</LastName>
<ForeName>Chun-Hsu</ForeName>
<Initials>CH</Initials>
<Identifier Source="ORCID">0000-0001-8700-583X</Identifier>
<AffiliationInfo><Affiliation>School of Pharmacy, Taipei Medical University, Taipei 11031, Taiwan. panch@tmu.edu.tw.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Lai</LastName>
<ForeName>Ming-Tsung</ForeName>
<Initials>MT</Initials>
<AffiliationInfo><Affiliation>Department of Pathology, Taichung Hospital, Ministry of Health and Welfare Taiwan, Taichung 40343, Taiwan. mtlailuke@gmail.com.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Lan</LastName>
<ForeName>Shou-Jen</ForeName>
<Initials>SJ</Initials>
<Identifier Source="ORCID">0000-0002-8395-2052</Identifier>
<AffiliationInfo><Affiliation>Department of Healthcare Administration, Asia University, Taichung 41354, Taiwan. sjlan@asia.edu.tw.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Wu</LastName>
<ForeName>Chieh-Hsi</ForeName>
<Initials>CH</Initials>
<AffiliationInfo><Affiliation>School of Pharmacy, Taipei Medical University, Taipei 11031, Taiwan. chhswu@tmu.edu.tw.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Sheu</LastName>
<ForeName>Ming-Jyh</ForeName>
<Initials>MJ</Initials>
<AffiliationInfo><Affiliation>School of Pharmacy, China Medical University, Taichung 40402, Taiwan. soybean13mtdtw@gmail.com.tw.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType>
</PublicationTypeList>
<ArticleDate DateType="Electronic"><Year>2018</Year>
<Month>03</Month>
<Day>09</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>3K9958V90M</RegistryNumber>
<NameOfSubstance UI="D000431">Ethanol</NameOfSubstance>
</Chemical>
</ChemicalList>
<CitationSubset>IM</CitationSubset>
<MeshHeadingList><MeshHeading><DescriptorName UI="D000072283" MajorTopicYN="N">A549 Cells</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D064591" MajorTopicYN="N">Allografts</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000970" MajorTopicYN="N">Antineoplastic Agents</DescriptorName>
<QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName>
<QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D055491" MajorTopicYN="N">Antrodia</DescriptorName>
<QualifierName UI="Q000737" MajorTopicYN="Y">chemistry</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D002465" MajorTopicYN="N">Cell Movement</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName>
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<Keyword MajorTopicYN="N">lung cancer</Keyword>
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	Serveur d'exploration sur la rapamycine et les champignons
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Serveur d'exploration sur la rapamycine et les champignons

Suppression of Cell Growth, Migration and Drug Resistance by Ethanolic Extract of Antrodia cinnamomea in Human Lung Cancer A549 Cells and C57BL/6J Allograft Tumor Model.

Suppression of Cell Growth, Migration and Drug Resistance by Ethanolic Extract of Antrodia cinnamomea in Human Lung Cancer A549 Cells and C57BL/6J Allograft Tumor Model.

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