Licarin A induces cell death by activation of autophagy and apoptosis in non-small cell lung cancer cells.
Identifieur interne : 000127 ( PubMed/Corpus ); précédent : 000126; suivant : 000128Licarin A induces cell death by activation of autophagy and apoptosis in non-small cell lung cancer cells.
Auteurs : Uma Maheswari ; Krishna Ghosh ; Sudha Rani SadrasSource :
- Apoptosis : an international journal on programmed cell death [ 1573-675X ] ; 2018.
English descriptors
- KwdEn :
- A549 Cells, Antineoplastic Agents, Phytogenic (pharmacology), Apoptosis (drug effects), Autophagy (drug effects), Beclin-1 (genetics), Beclin-1 (metabolism), Carcinoma, Non-Small-Cell Lung (drug therapy), Carcinoma, Non-Small-Cell Lung (genetics), Carcinoma, Non-Small-Cell Lung (metabolism), Carcinoma, Non-Small-Cell Lung (physiopathology), Caspase 3 (genetics), Caspase 3 (metabolism), Humans, Lignans (pharmacology), Lung Neoplasms (genetics), Lung Neoplasms (metabolism), Lung Neoplasms (physiopathology), Myristica (chemistry), Peroxisome Proliferator-Activated Receptors (genetics), Peroxisome Proliferator-Activated Receptors (metabolism), Plant Extracts (pharmacology), Reactive Oxygen Species (metabolism).
- MESH :
- chemical , genetics : Beclin-1, Caspase 3, Peroxisome Proliferator-Activated Receptors.
- chemical , metabolism : Beclin-1, Caspase 3, Peroxisome Proliferator-Activated Receptors, Reactive Oxygen Species.
- chemical , pharmacology : Antineoplastic Agents, Phytogenic, Lignans, Plant Extracts.
- chemistry : Myristica.
- drug effects : Apoptosis, Autophagy.
- drug therapy : Carcinoma, Non-Small-Cell Lung.
- genetics : Carcinoma, Non-Small-Cell Lung, Lung Neoplasms.
- metabolism : Carcinoma, Non-Small-Cell Lung, Lung Neoplasms.
- physiopathology : Carcinoma, Non-Small-Cell Lung, Lung Neoplasms.
- A549 Cells, Humans.
Abstract
Lung cancer has a relatively poor prognosis with a low survival rate and drugs that target other cell death mechanism like autophagy may help improving current therapeutic strategy. This study investigated the anti-proliferative effect of Licarin A (LCA) from Myristica fragrans in non-small cell lung cancer cell lines-A549, NCI-H23, NCI-H520 and NCI-H460. LCA inhibited proliferation of all the four cell lines in a dose and time dependent manner with minimum IC50 of 20.03 ± 3.12, 22.19 ± 1.37 µM in NCI-H23 and A549 cells respectively. Hence NCI-H23 and A549 cells were used to assess the ability LCA to induce autophagy and apoptosis. LCA treatment caused G1 arrest, increase in Beclin 1, LC3II levels and degradation of p62 indicating activation of autophagy in both NCI-H23 and A549 cells. In addition, LCA mediated apoptotic cell death was confirmed by MMP loss, increased ROS, cleaved PARP and decreased pro-caspase3. To understand the role of LCA induced autophagy and its association with apoptosis, cells were analysed following treatment with a late autophagy inhibitor-chloroquine and also after Beclin 1 siRNA transfection. Data indicated that inhibition of autophagy resulted in reduced anti-proliferative as well as pro-apoptotic ability of LCA. These findings confirmed that LCA brought about autophagy dependent apoptosis in non-small cell lung cancer cells and hence it may serve as a potential drug candidate for non-small cell lung cancer therapy.
DOI: 10.1007/s10495-018-1449-8
PubMed: 29468481
Links to Exploration step
pubmed:29468481Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Licarin A induces cell death by activation of autophagy and apoptosis in non-small cell lung cancer cells.</title><author><name sortKey="Maheswari, Uma" sort="Maheswari, Uma" uniqKey="Maheswari U" first="Uma" last="Maheswari">Uma Maheswari</name><affiliation><nlm:affiliation>DBT-IPLS Programme, Department of Biochemistry and Molecular Biology, Pondicherry University, Pondicherry, 605014, India.</nlm:affiliation></affiliation></author><author><name sortKey="Ghosh, Krishna" sort="Ghosh, Krishna" uniqKey="Ghosh K" first="Krishna" last="Ghosh">Krishna Ghosh</name><affiliation><nlm:affiliation>Department of Biochemistry and Molecular Biology, Central University of Kerala, Kasaragod, Kerala, 671314, India.</nlm:affiliation></affiliation></author><author><name sortKey="Sadras, Sudha Rani" sort="Sadras, Sudha Rani" uniqKey="Sadras S" first="Sudha Rani" last="Sadras">Sudha Rani Sadras</name><affiliation><nlm:affiliation>DBT-IPLS Programme, Department of Biochemistry and Molecular Biology, Pondicherry University, Pondicherry, 605014, India. dr.ssrlab@gmail.com.</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2018">2018</date><idno type="RBID">pubmed:29468481</idno><idno type="pmid">29468481</idno><idno type="doi">10.1007/s10495-018-1449-8</idno><idno type="wicri:Area/PubMed/Corpus">000127</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000127</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Licarin A induces cell death by activation of autophagy and apoptosis in non-small cell lung cancer cells.</title><author><name sortKey="Maheswari, Uma" sort="Maheswari, Uma" uniqKey="Maheswari U" first="Uma" last="Maheswari">Uma Maheswari</name><affiliation><nlm:affiliation>DBT-IPLS Programme, Department of Biochemistry and Molecular Biology, Pondicherry University, Pondicherry, 605014, India.</nlm:affiliation></affiliation></author><author><name sortKey="Ghosh, Krishna" sort="Ghosh, Krishna" uniqKey="Ghosh K" first="Krishna" last="Ghosh">Krishna Ghosh</name><affiliation><nlm:affiliation>Department of Biochemistry and Molecular Biology, Central University of Kerala, Kasaragod, Kerala, 671314, India.</nlm:affiliation></affiliation></author><author><name sortKey="Sadras, Sudha Rani" sort="Sadras, Sudha Rani" uniqKey="Sadras S" first="Sudha Rani" last="Sadras">Sudha Rani Sadras</name><affiliation><nlm:affiliation>DBT-IPLS Programme, Department of Biochemistry and Molecular Biology, Pondicherry University, Pondicherry, 605014, India. dr.ssrlab@gmail.com.</nlm:affiliation></affiliation></author></analytic><series><title level="j">Apoptosis : an international journal on programmed cell death</title><idno type="eISSN">1573-675X</idno><imprint><date when="2018" type="published">2018</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>A549 Cells</term><term>Antineoplastic Agents, Phytogenic (pharmacology)</term><term>Apoptosis (drug effects)</term><term>Autophagy (drug effects)</term><term>Beclin-1 (genetics)</term><term>Beclin-1 (metabolism)</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 (physiopathology)</term><term>Caspase 3 (genetics)</term><term>Caspase 3 (metabolism)</term><term>Humans</term><term>Lignans (pharmacology)</term><term>Lung Neoplasms (genetics)</term><term>Lung Neoplasms (metabolism)</term><term>Lung Neoplasms (physiopathology)</term><term>Myristica (chemistry)</term><term>Peroxisome Proliferator-Activated Receptors (genetics)</term><term>Peroxisome Proliferator-Activated Receptors (metabolism)</term><term>Plant Extracts (pharmacology)</term><term>Reactive Oxygen Species (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Beclin-1</term><term>Caspase 3</term><term>Peroxisome Proliferator-Activated Receptors</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Beclin-1</term><term>Caspase 3</term><term>Peroxisome Proliferator-Activated Receptors</term><term>Reactive Oxygen Species</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Antineoplastic Agents, Phytogenic</term><term>Lignans</term><term>Plant Extracts</term></keywords><keywords scheme="MESH" qualifier="chemistry" xml:lang="en"><term>Myristica</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>Carcinoma, Non-Small-Cell Lung</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>Lung Neoplasms</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Carcinoma, Non-Small-Cell Lung</term><term>Lung Neoplasms</term></keywords><keywords scheme="MESH" xml:lang="en"><term>A549 Cells</term><term>Humans</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Lung cancer has a relatively poor prognosis with a low survival rate and drugs that target other cell death mechanism like autophagy may help improving current therapeutic strategy. This study investigated the anti-proliferative effect of Licarin A (LCA) from Myristica fragrans in non-small cell lung cancer cell lines-A549, NCI-H23, NCI-H520 and NCI-H460. LCA inhibited proliferation of all the four cell lines in a dose and time dependent manner with minimum IC50 of 20.03 ± 3.12, 22.19 ± 1.37 µM in NCI-H23 and A549 cells respectively. Hence NCI-H23 and A549 cells were used to assess the ability LCA to induce autophagy and apoptosis. LCA treatment caused G1 arrest, increase in Beclin 1, LC3II levels and degradation of p62 indicating activation of autophagy in both NCI-H23 and A549 cells. In addition, LCA mediated apoptotic cell death was confirmed by MMP loss, increased ROS, cleaved PARP and decreased pro-caspase3. To understand the role of LCA induced autophagy and its association with apoptosis, cells were analysed following treatment with a late autophagy inhibitor-chloroquine and also after Beclin 1 siRNA transfection. Data indicated that inhibition of autophagy resulted in reduced anti-proliferative as well as pro-apoptotic ability of LCA. These findings confirmed that LCA brought about autophagy dependent apoptosis in non-small cell lung cancer cells and hence it may serve as a potential drug candidate for non-small cell lung cancer therapy.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">29468481</PMID><DateCompleted><Year>2019</Year><Month>09</Month><Day>23</Day></DateCompleted><DateRevised><Year>2019</Year><Month>09</Month><Day>23</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1573-675X</ISSN><JournalIssue CitedMedium="Internet"><Volume>23</Volume><Issue>3-4</Issue><PubDate><Year>2018</Year><Month>04</Month></PubDate></JournalIssue><Title>Apoptosis : an international journal on programmed cell death</Title><ISOAbbreviation>Apoptosis</ISOAbbreviation></Journal><ArticleTitle>Licarin A induces cell death by activation of autophagy and apoptosis in non-small cell lung cancer cells.</ArticleTitle><Pagination><MedlinePgn>210-225</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1007/s10495-018-1449-8</ELocationID><Abstract><AbstractText>Lung cancer has a relatively poor prognosis with a low survival rate and drugs that target other cell death mechanism like autophagy may help improving current therapeutic strategy. This study investigated the anti-proliferative effect of Licarin A (LCA) from Myristica fragrans in non-small cell lung cancer cell lines-A549, NCI-H23, NCI-H520 and NCI-H460. LCA inhibited proliferation of all the four cell lines in a dose and time dependent manner with minimum IC50 of 20.03 ± 3.12, 22.19 ± 1.37 µM in NCI-H23 and A549 cells respectively. Hence NCI-H23 and A549 cells were used to assess the ability LCA to induce autophagy and apoptosis. LCA treatment caused G1 arrest, increase in Beclin 1, LC3II levels and degradation of p62 indicating activation of autophagy in both NCI-H23 and A549 cells. In addition, LCA mediated apoptotic cell death was confirmed by MMP loss, increased ROS, cleaved PARP and decreased pro-caspase3. To understand the role of LCA induced autophagy and its association with apoptosis, cells were analysed following treatment with a late autophagy inhibitor-chloroquine and also after Beclin 1 siRNA transfection. Data indicated that inhibition of autophagy resulted in reduced anti-proliferative as well as pro-apoptotic ability of LCA. These findings confirmed that LCA brought about autophagy dependent apoptosis in non-small cell lung cancer cells and hence it may serve as a potential drug candidate for non-small cell lung cancer therapy.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Maheswari</LastName><ForeName>Uma</ForeName><Initials>U</Initials><AffiliationInfo><Affiliation>DBT-IPLS Programme, Department of Biochemistry and Molecular Biology, Pondicherry University, Pondicherry, 605014, India.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ghosh</LastName><ForeName>Krishna</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Department of Biochemistry and Molecular Biology, Central University of Kerala, Kasaragod, Kerala, 671314, India.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sadras</LastName><ForeName>Sudha Rani</ForeName><Initials>SR</Initials><Identifier Source="ORCID">0000-0002-5643-4065</Identifier><AffiliationInfo><Affiliation>DBT-IPLS Programme, Department of Biochemistry and Molecular Biology, Pondicherry University, Pondicherry, 605014, India. dr.ssrlab@gmail.com.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Biochemistry and Molecular Biology, School of Life Sciences, Pondicherry University, Pondicherry, 605014, India. dr.ssrlab@gmail.com.</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></Article><MedlineJournalInfo><Country>Netherlands</Country><MedlineTA>Apoptosis</MedlineTA><NlmUniqueID>9712129</NlmUniqueID><ISSNLinking>1360-8185</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000972">Antineoplastic Agents, Phytogenic</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="D017705">Lignans</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D047492">Peroxisome Proliferator-Activated Receptors</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D010936">Plant Extracts</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D017382">Reactive Oxygen Species</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C432503">licarin A</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.4.22.-</RegistryNumber><NameOfSubstance UI="D053148">Caspase 3</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="ErratumIn"><RefSource>Apoptosis. 2018 Mar 15;:</RefSource><PMID Version="1">29546663</PMID></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName UI="D000072283" MajorTopicYN="N">A549 Cells</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="Y">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001343" MajorTopicYN="N">Autophagy</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000071186" MajorTopicYN="N">Beclin-1</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002289" MajorTopicYN="N">Carcinoma, Non-Small-Cell Lung</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D053148" MajorTopicYN="N">Caspase 3</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017705" MajorTopicYN="N">Lignans</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008175" MajorTopicYN="N">Lung Neoplasms</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D026323" MajorTopicYN="N">Myristica</DescriptorName><QualifierName UI="Q000737" MajorTopicYN="Y">chemistry</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D047492" MajorTopicYN="N">Peroxisome Proliferator-Activated Receptors</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010936" MajorTopicYN="N">Plant Extracts</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</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="Y">Apoptosis</Keyword><Keyword MajorTopicYN="Y">Autophagy</Keyword><Keyword MajorTopicYN="Y">Chloroquine</Keyword><Keyword MajorTopicYN="Y">Licarin A</Keyword><Keyword MajorTopicYN="Y">Reactive oxygen species</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2018</Year><Month>2</Month><Day>23</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2019</Year><Month>9</Month><Day>24</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2018</Year><Month>2</Month><Day>23</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">29468481</ArticleId><ArticleId IdType="doi">10.1007/s10495-018-1449-8</ArticleId><ArticleId IdType="pii">10.1007/s10495-018-1449-8</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Sante/explor/ChloroquineV1/Data/PubMed/Corpus
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000127 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/PubMed/Corpus/biblio.hfd -nk 000127 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Sante
|area= ChloroquineV1
|flux= PubMed
|étape= Corpus
|type= RBID
|clé= pubmed:29468481
|texte= Licarin A induces cell death by activation of autophagy and apoptosis in non-small cell lung cancer cells.
}}
Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/PubMed/Corpus/RBID.i -Sk "pubmed:29468481" \
| HfdSelect -Kh $EXPLOR_AREA/Data/PubMed/Corpus/biblio.hfd \
| NlmPubMed2Wicri -a ChloroquineV1
| This area was generated with Dilib version V0.6.33. |  |