Autophagy inhibition enhances isorhamnetin‑induced mitochondria‑dependent apoptosis in non‑small cell lung cancer cells.
Identifieur interne : 000240 ( PubMed/Corpus ); précédent : 000239; suivant : 000241Autophagy inhibition enhances isorhamnetin‑induced mitochondria‑dependent apoptosis in non‑small cell lung cancer cells.
Auteurs : Yushu Ruan ; Ke Hu ; Hongbo ChenSource :
- Molecular medicine reports [ 1791-3004 ] ; 2015.
English descriptors
- KwdEn :
- Adenine (analogs & derivatives), Adenine (pharmacology), Animals, Antineoplastic Agents, Phytogenic (pharmacology), Apoptosis (drug effects), Autophagy (drug effects), Carcinoma, Non-Small-Cell Lung (drug therapy), Carcinoma, Non-Small-Cell Lung (genetics), Carcinoma, Non-Small-Cell Lung (metabolism), Carcinoma, Non-Small-Cell Lung (pathology), Caspases (genetics), Caspases (metabolism), Cell Line, Tumor, Cell Proliferation (drug effects), Cytochromes c (metabolism), Dose-Response Relationship, Drug, Drug Synergism, Epithelial Cells (drug effects), Epithelial Cells (metabolism), Epithelial Cells (pathology), Gene Expression, Humans, Hydroxychloroquine (pharmacology), Lung Neoplasms (drug therapy), Lung Neoplasms (genetics), Lung Neoplasms (metabolism), Lung Neoplasms (pathology), Membrane Potential, Mitochondrial (drug effects), Mice, Mice, Nude, Microtubule-Associated Proteins (genetics), Microtubule-Associated Proteins (metabolism), Mitochondria (drug effects), Mitochondria (metabolism), Quercetin (analogs & derivatives), Quercetin (pharmacology), Xenograft Model Antitumor Assays.
- MESH :
- chemical , analogs & derivatives : Adenine, Quercetin.
- chemical , genetics : Caspases, Microtubule-Associated Proteins.
- chemical , metabolism : Caspases, Cytochromes c, Microtubule-Associated Proteins.
- chemical , pharmacology : Adenine, Antineoplastic Agents, Phytogenic, Hydroxychloroquine, Quercetin.
- drug effects : Apoptosis, Autophagy, Cell Proliferation, Epithelial Cells, Membrane Potential, Mitochondrial, Mitochondria.
- drug therapy : Carcinoma, Non-Small-Cell Lung, Lung Neoplasms.
- genetics : Carcinoma, Non-Small-Cell Lung, Lung Neoplasms.
- metabolism : Carcinoma, Non-Small-Cell Lung, Epithelial Cells, Lung Neoplasms, Mitochondria.
- pathology : Carcinoma, Non-Small-Cell Lung, Epithelial Cells, Lung Neoplasms.
- Animals, Cell Line, Tumor, Dose-Response Relationship, Drug, Drug Synergism, Gene Expression, Humans, Mice, Mice, Nude, Xenograft Model Antitumor Assays.
Abstract
Isorhamnetin (ISO) is a flavonoid from plants of the Polygonaceae family and is also an immediate metabolite of quercetin in mammals. To date, the anti‑tumor effects of ISO and the underlying mechanisms have not been elucidated in lung cancer cells. The present study investigated the inhibitory effects of ISO on the growth of human lung cancer A549 cells. Treatment of the lung cancer cells with ISO significantly suppressed cell proliferation and colony formation. ISO treatment also resulted in a significant increase in apoptotic cell death of A549 cells in a time- and dose-dependent manner. Further investigation showed that the apoptosis proceeded via the mitochondria‑dependent pathway as indicated by alteration of the mitochondrial membrane potential, the release of cytochrome C and caspase activation. Of note, treatment with ISO also induced the formation of autophagosomes and light chain 3‑II protein in A549 cells. Furthermore, co‑treatment with autophagy inhibitors 3‑methyladenine and hydroxychloroquine significantly inhibited the ISO‑induced autophagy and enhanced the ISO‑induced apoptotic cell death in vitro as well as in vivo. Thus, the results of the present study suggested that ISO is a potential anti‑lung cancer agent. In addition, the results indicated that the inhibition of autophagy may be a useful strategy for enhancing the chemotherapeutic effect of ISO on lung cancer cells.
DOI: 10.3892/mmr.2015.4148
PubMed: 26238746
Links to Exploration step
pubmed:26238746Le document en format XML
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China.</nlm:affiliation></affiliation></author><author><name sortKey="Chen, Hongbo" sort="Chen, Hongbo" uniqKey="Chen H" first="Hongbo" last="Chen">Hongbo Chen</name><affiliation><nlm:affiliation>The Shenzhen Key Lab of Gene and Antibody Therapy, Division of Life and Health Sciences, Shenzhen Graduate School of Tsinghua University, Shenzhen, Guangdong 518055, P.R. China.</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2015">2015</date><idno type="RBID">pubmed:26238746</idno><idno type="pmid">26238746</idno><idno type="doi">10.3892/mmr.2015.4148</idno><idno type="wicri:Area/PubMed/Corpus">000240</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000240</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Autophagy inhibition enhances isorhamnetin‑induced mitochondria‑dependent apoptosis in non‑small cell lung cancer cells.</title><author><name sortKey="Ruan, Yushu" sort="Ruan, Yushu" uniqKey="Ruan Y" first="Yushu" last="Ruan">Yushu Ruan</name><affiliation><nlm:affiliation>Division of Respiratory Disease, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, P.R. China.</nlm:affiliation></affiliation></author><author><name sortKey="Hu, Ke" sort="Hu, Ke" uniqKey="Hu K" first="Ke" last="Hu">Ke Hu</name><affiliation><nlm:affiliation>Division of Respiratory Disease, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, P.R. China.</nlm:affiliation></affiliation></author><author><name sortKey="Chen, Hongbo" sort="Chen, Hongbo" uniqKey="Chen H" first="Hongbo" last="Chen">Hongbo Chen</name><affiliation><nlm:affiliation>The Shenzhen Key Lab of Gene and Antibody Therapy, Division of Life and Health Sciences, Shenzhen Graduate School of Tsinghua University, Shenzhen, Guangdong 518055, P.R. China.</nlm:affiliation></affiliation></author></analytic><series><title level="j">Molecular medicine reports</title><idno type="eISSN">1791-3004</idno><imprint><date when="2015" type="published">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adenine (analogs & derivatives)</term><term>Adenine (pharmacology)</term><term>Animals</term><term>Antineoplastic Agents, Phytogenic (pharmacology)</term><term>Apoptosis (drug effects)</term><term>Autophagy (drug effects)</term><term>Carcinoma, Non-Small-Cell Lung (drug therapy)</term><term>Carcinoma, Non-Small-Cell Lung (genetics)</term><term>Carcinoma, Non-Small-Cell Lung (metabolism)</term><term>Carcinoma, Non-Small-Cell Lung (pathology)</term><term>Caspases (genetics)</term><term>Caspases (metabolism)</term><term>Cell Line, Tumor</term><term>Cell Proliferation (drug effects)</term><term>Cytochromes c (metabolism)</term><term>Dose-Response Relationship, Drug</term><term>Drug Synergism</term><term>Epithelial Cells (drug effects)</term><term>Epithelial Cells (metabolism)</term><term>Epithelial Cells (pathology)</term><term>Gene Expression</term><term>Humans</term><term>Hydroxychloroquine (pharmacology)</term><term>Lung Neoplasms (drug therapy)</term><term>Lung Neoplasms (genetics)</term><term>Lung Neoplasms (metabolism)</term><term>Lung Neoplasms (pathology)</term><term>Membrane Potential, Mitochondrial (drug effects)</term><term>Mice</term><term>Mice, Nude</term><term>Microtubule-Associated Proteins (genetics)</term><term>Microtubule-Associated Proteins (metabolism)</term><term>Mitochondria (drug effects)</term><term>Mitochondria (metabolism)</term><term>Quercetin (analogs & derivatives)</term><term>Quercetin (pharmacology)</term><term>Xenograft Model Antitumor Assays</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analogs & derivatives" xml:lang="en"><term>Adenine</term><term>Quercetin</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Caspases</term><term>Microtubule-Associated Proteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Caspases</term><term>Cytochromes c</term><term>Microtubule-Associated Proteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Adenine</term><term>Antineoplastic Agents, Phytogenic</term><term>Hydroxychloroquine</term><term>Quercetin</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Apoptosis</term><term>Autophagy</term><term>Cell Proliferation</term><term>Epithelial Cells</term><term>Membrane Potential, Mitochondrial</term><term>Mitochondria</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Carcinoma, Non-Small-Cell Lung</term><term>Lung Neoplasms</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Carcinoma, Non-Small-Cell Lung</term><term>Lung Neoplasms</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Carcinoma, Non-Small-Cell Lung</term><term>Epithelial Cells</term><term>Lung Neoplasms</term><term>Mitochondria</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Carcinoma, Non-Small-Cell Lung</term><term>Epithelial Cells</term><term>Lung Neoplasms</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Cell Line, Tumor</term><term>Dose-Response Relationship, Drug</term><term>Drug Synergism</term><term>Gene Expression</term><term>Humans</term><term>Mice</term><term>Mice, Nude</term><term>Xenograft Model Antitumor Assays</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Isorhamnetin (ISO) is a flavonoid from plants of the Polygonaceae family and is also an immediate metabolite of quercetin in mammals. To date, the anti‑tumor effects of ISO and the underlying mechanisms have not been elucidated in lung cancer cells. The present study investigated the inhibitory effects of ISO on the growth of human lung cancer A549 cells. Treatment of the lung cancer cells with ISO significantly suppressed cell proliferation and colony formation. ISO treatment also resulted in a significant increase in apoptotic cell death of A549 cells in a time- and dose-dependent manner. Further investigation showed that the apoptosis proceeded via the mitochondria‑dependent pathway as indicated by alteration of the mitochondrial membrane potential, the release of cytochrome C and caspase activation. Of note, treatment with ISO also induced the formation of autophagosomes and light chain 3‑II protein in A549 cells. Furthermore, co‑treatment with autophagy inhibitors 3‑methyladenine and hydroxychloroquine significantly inhibited the ISO‑induced autophagy and enhanced the ISO‑induced apoptotic cell death in vitro as well as in vivo. Thus, the results of the present study suggested that ISO is a potential anti‑lung cancer agent. In addition, the results indicated that the inhibition of autophagy may be a useful strategy for enhancing the chemotherapeutic effect of ISO on lung cancer cells.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">26238746</PMID><DateCompleted><Year>2016</Year><Month>06</Month><Day>23</Day></DateCompleted><DateRevised><Year>2018</Year><Month>12</Month><Day>02</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1791-3004</ISSN><JournalIssue CitedMedium="Internet"><Volume>12</Volume><Issue>4</Issue><PubDate><Year>2015</Year><Month>Oct</Month></PubDate></JournalIssue><Title>Molecular medicine reports</Title><ISOAbbreviation>Mol Med Rep</ISOAbbreviation></Journal><ArticleTitle>Autophagy inhibition enhances isorhamnetin‑induced mitochondria‑dependent apoptosis in non‑small cell lung cancer cells.</ArticleTitle><Pagination><MedlinePgn>5796-806</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.3892/mmr.2015.4148</ELocationID><Abstract><AbstractText>Isorhamnetin (ISO) is a flavonoid from plants of the Polygonaceae family and is also an immediate metabolite of quercetin in mammals. To date, the anti‑tumor effects of ISO and the underlying mechanisms have not been elucidated in lung cancer cells. The present study investigated the inhibitory effects of ISO on the growth of human lung cancer A549 cells. Treatment of the lung cancer cells with ISO significantly suppressed cell proliferation and colony formation. ISO treatment also resulted in a significant increase in apoptotic cell death of A549 cells in a time- and dose-dependent manner. Further investigation showed that the apoptosis proceeded via the mitochondria‑dependent pathway as indicated by alteration of the mitochondrial membrane potential, the release of cytochrome C and caspase activation. Of note, treatment with ISO also induced the formation of autophagosomes and light chain 3‑II protein in A549 cells. Furthermore, co‑treatment with autophagy inhibitors 3‑methyladenine and hydroxychloroquine significantly inhibited the ISO‑induced autophagy and enhanced the ISO‑induced apoptotic cell death in vitro as well as in vivo. Thus, the results of the present study suggested that ISO is a potential anti‑lung cancer agent. In addition, the results indicated that the inhibition of autophagy may be a useful strategy for enhancing the chemotherapeutic effect of ISO on lung cancer cells.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Ruan</LastName><ForeName>Yushu</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Division of Respiratory Disease, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, P.R. China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hu</LastName><ForeName>Ke</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Division of Respiratory Disease, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, P.R. China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chen</LastName><ForeName>Hongbo</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>The Shenzhen Key Lab of Gene and Antibody Therapy, Division of Life and Health Sciences, Shenzhen Graduate School of Tsinghua University, Shenzhen, Guangdong 518055, P.R. China.</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>2015</Year><Month>07</Month><Day>29</Day></ArticleDate></Article><MedlineJournalInfo><Country>Greece</Country><MedlineTA>Mol Med Rep</MedlineTA><NlmUniqueID>101475259</NlmUniqueID><ISSNLinking>1791-2997</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000972">Antineoplastic Agents, Phytogenic</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C477012">MAP1LC3A protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D008869">Microtubule-Associated 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UI="D000225">Adenine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000225" MajorTopicYN="N">Adenine</DescriptorName><QualifierName UI="Q000031" MajorTopicYN="Y">analogs & derivatives</QualifierName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000972" MajorTopicYN="N">Antineoplastic Agents, Phytogenic</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017209" MajorTopicYN="N">Apoptosis</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001343" MajorTopicYN="N">Autophagy</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug 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MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008928" MajorTopicYN="N">Mitochondria</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011794" MajorTopicYN="N">Quercetin</DescriptorName><QualifierName UI="Q000031" MajorTopicYN="Y">analogs & derivatives</QualifierName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D023041" MajorTopicYN="N">Xenograft Model Antitumor Assays</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2015</Year><Month>04</Month><Day>02</Day></PubMedPubDate><PubMedPubDate 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