Links to Exploration step
Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Ecliptasaponin A induces apoptosis through the activation of ASK1/JNK pathway and autophagy in human lung cancer cells</title><author><name sortKey="Han, Jia" sort="Han, Jia" uniqKey="Han J" first="Jia" last="Han">Jia Han</name></author><author><name sortKey="Lv, Wang" sort="Lv, Wang" uniqKey="Lv W" first="Wang" last="Lv">Wang Lv</name></author><author><name sortKey="Sheng, Hongxu" sort="Sheng, Hongxu" uniqKey="Sheng H" first="Hongxu" last="Sheng">Hongxu Sheng</name></author><author><name sortKey="Wang, Yiqing" sort="Wang, Yiqing" uniqKey="Wang Y" first="Yiqing" last="Wang">Yiqing Wang</name></author><author><name sortKey="Cao, Longxiang" sort="Cao, Longxiang" uniqKey="Cao L" first="Longxiang" last="Cao">Longxiang Cao</name></author><author><name sortKey="Huang, Sha" sort="Huang, Sha" uniqKey="Huang S" first="Sha" last="Huang">Sha Huang</name></author><author><name sortKey="Zhu, Linhai" sort="Zhu, Linhai" uniqKey="Zhu L" first="Linhai" last="Zhu">Linhai Zhu</name></author><author><name sortKey="Hu, Jian" sort="Hu, Jian" uniqKey="Hu J" first="Jian" last="Hu">Jian Hu</name></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">31807521</idno><idno type="pmc">6861768</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6861768</idno><idno type="RBID">PMC:6861768</idno><idno type="doi">10.21037/atm.2019.10.07</idno><date when="2019">2019</date><idno type="wicri:Area/Pmc/Corpus">000358</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000358</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Ecliptasaponin A induces apoptosis through the activation of ASK1/JNK pathway and autophagy in human lung cancer cells</title><author><name sortKey="Han, Jia" sort="Han, Jia" uniqKey="Han J" first="Jia" last="Han">Jia Han</name></author><author><name sortKey="Lv, Wang" sort="Lv, Wang" uniqKey="Lv W" first="Wang" last="Lv">Wang Lv</name></author><author><name sortKey="Sheng, Hongxu" sort="Sheng, Hongxu" uniqKey="Sheng H" first="Hongxu" last="Sheng">Hongxu Sheng</name></author><author><name sortKey="Wang, Yiqing" sort="Wang, Yiqing" uniqKey="Wang Y" first="Yiqing" last="Wang">Yiqing Wang</name></author><author><name sortKey="Cao, Longxiang" sort="Cao, Longxiang" uniqKey="Cao L" first="Longxiang" last="Cao">Longxiang Cao</name></author><author><name sortKey="Huang, Sha" sort="Huang, Sha" uniqKey="Huang S" first="Sha" last="Huang">Sha Huang</name></author><author><name sortKey="Zhu, Linhai" sort="Zhu, Linhai" uniqKey="Zhu L" first="Linhai" last="Zhu">Linhai Zhu</name></author><author><name sortKey="Hu, Jian" sort="Hu, Jian" uniqKey="Hu J" first="Jian" last="Hu">Jian Hu</name></author></analytic><series><title level="j">Annals of Translational Medicine</title><idno type="ISSN">2305-5839</idno><idno type="eISSN">2305-5847</idno><imprint><date when="2019">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><sec><title>Background</title><p>Non-small cell lung cancer (NSCLC) is one of the causes of carcinomas mortality worldwide. Ecliptasaponin A (ES), a natural product extracted from the plant known as Eclipta prostrata, has been reported as an anti-cancer drug against various cancer cell lines. However, the exact mechanisms of ES have not yet been fully characterized.</p></sec><sec><title>Methods</title><p>Numerous studies have been done to support that ES has a powerful inhibiting effect on the growth of cancers via the activation of apoptosis and autophagy. To explore the underlying mechanisms of anti-cancer and investigate the relationships of the apoptosis and autophagy, we used apoptosis signal-regulating kinase 1 (ASK1) inhibitor (GS-4997), c-Jun N-terminal kinase (JNK) inhibitor (SP600125), and autophagy inhibitor [chloroquine (CQ) and 3-methyladenine (3-MA)].</p></sec><sec><title>Results</title><p>ES could potently suppress cell viability and induces apoptotic cell death of human lung cancer cells H460 and H1975. ES activated apoptosis via ASK1/JNK pathway, GS-4997 and SP600125 can attenuated these effects. Furthermore, ES could triggered autophagy in lung cancer cell lines, and the autophagy inhibitor 3-MA and CQ reversed ES-induced apoptosis in H460 and H1975 cells. Furthermore, SP600125 can inhibit autophagy.</p></sec><sec><title>Conclusions</title><p>This study showed that ES induces apoptosis in human lung cancer cells by triggering enhanced autophagy and ASK1/JNK pathway, which may thus be a promising agent against lung cancer.</p></sec></div></front></TEI><pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Ann Transl Med</journal-id><journal-id journal-id-type="iso-abbrev">Ann Transl Med</journal-id><journal-id journal-id-type="publisher-id">ATM</journal-id><journal-title-group><journal-title>Annals of Translational Medicine</journal-title></journal-title-group><issn pub-type="ppub">2305-5839</issn><issn pub-type="epub">2305-5847</issn><publisher><publisher-name>AME Publishing Company</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">31807521</article-id><article-id pub-id-type="pmc">6861768</article-id><article-id pub-id-type="publisher-id">atm-07-20-539</article-id><article-id pub-id-type="doi">10.21037/atm.2019.10.07</article-id><article-categories><subj-group subj-group-type="heading"><subject>Original Article</subject></subj-group></article-categories><title-group><article-title>Ecliptasaponin A induces apoptosis through the activation of ASK1/JNK pathway and autophagy in human lung cancer cells</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Han</surname><given-names>Jia</given-names></name></contrib><contrib contrib-type="author"><name><surname>Lv</surname><given-names>Wang</given-names></name></contrib><contrib contrib-type="author"><name><surname>Sheng</surname><given-names>Hongxu</given-names></name></contrib><contrib contrib-type="author"><name><surname>Wang</surname><given-names>Yiqing</given-names></name></contrib><contrib contrib-type="author"><name><surname>Cao</surname><given-names>Longxiang</given-names></name></contrib><contrib contrib-type="author"><name><surname>Huang</surname><given-names>Sha</given-names></name></contrib><contrib contrib-type="author"><name><surname>Zhu</surname><given-names>Linhai</given-names></name></contrib><contrib contrib-type="author" corresp="yes"><name><surname>Hu</surname><given-names>Jian</given-names></name></contrib><aff id="aff1">Department of Thoracic Surgery, The First Affiliated Hospital, School of Medicine,<institution>Zhejiang University</institution>,<addr-line>Hangzhou 310003</addr-line>,<country>China</country></aff></contrib-group><author-notes><fn id="afn1"><p><italic>Contributions:</italic> (I) Conception and design: J Han, J Hu; (II) Administrative support: W Lv, Y Wang; (III) Provision of study materials or patients: J Han, H Sheng; (IV) Collection and assembly of data: J Han, L Cao; (V) Data analysis and interpretation: All authors; (VI) Manuscript writing: All authors; (VII) Final approval of manuscript: All authors.</p></fn><corresp id="cor1"><italic>Correspondence to:</italic> Jian Hu. Department of Thoracic Surgery, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou 310003, China. Email: <email xlink:href="dr_hujian@zju.edu.cn">dr_hujian@zju.edu.cn</email>.</corresp><fn fn-type="COI-statement"><p><italic>Conflicts of Interest:</italic> The authors have no conflicts of interest to declare.</p></fn></author-notes><pub-date pub-type="epub-ppub"><month>10</month><year>2019</year></pub-date><pmc-comment>Fake ppub date generated by PMC from publisher
pub-date/@pub-type='epub-ppub' </pmc-comment>
<pub-date pub-type="ppub"><month>10</month><year>2019</year></pub-date><volume>7</volume><issue>20</issue><elocation-id>539</elocation-id><history><date date-type="received"><day>10</day><month>9</month><year>2019</year></date><date date-type="accepted"><day>25</day><month>9</month><year>2019</year></date></history><permissions><copyright-statement>2019 Annals of Translational Medicine. All rights reserved.</copyright-statement><copyright-year>2019</copyright-year><copyright-holder>Annals of Translational Medicine.</copyright-holder></permissions><abstract><sec><title>Background</title><p>Non-small cell lung cancer (NSCLC) is one of the causes of carcinomas mortality worldwide. Ecliptasaponin A (ES), a natural product extracted from the plant known as Eclipta prostrata, has been reported as an anti-cancer drug against various cancer cell lines. However, the exact mechanisms of ES have not yet been fully characterized.</p></sec><sec><title>Methods</title><p>Numerous studies have been done to support that ES has a powerful inhibiting effect on the growth of cancers via the activation of apoptosis and autophagy. To explore the underlying mechanisms of anti-cancer and investigate the relationships of the apoptosis and autophagy, we used apoptosis signal-regulating kinase 1 (ASK1) inhibitor (GS-4997), c-Jun N-terminal kinase (JNK) inhibitor (SP600125), and autophagy inhibitor [chloroquine (CQ) and 3-methyladenine (3-MA)].</p></sec><sec><title>Results</title><p>ES could potently suppress cell viability and induces apoptotic cell death of human lung cancer cells H460 and H1975. ES activated apoptosis via ASK1/JNK pathway, GS-4997 and SP600125 can attenuated these effects. Furthermore, ES could triggered autophagy in lung cancer cell lines, and the autophagy inhibitor 3-MA and CQ reversed ES-induced apoptosis in H460 and H1975 cells. Furthermore, SP600125 can inhibit autophagy.</p></sec><sec><title>Conclusions</title><p>This study showed that ES induces apoptosis in human lung cancer cells by triggering enhanced autophagy and ASK1/JNK pathway, which may thus be a promising agent against lung cancer.</p></sec></abstract><kwd-group kwd-group-type="author"><title>Keywords: </title><kwd>Lung cancer</kwd><kwd>Ecliptasaponin A (ES)</kwd><kwd>apoptosis signal-regulating kinase 1 (ASK1)</kwd><kwd>c-Jun N-terminal kinase (JNK)</kwd><kwd>autophagy</kwd><kwd>apoptosis</kwd></kwd-group></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Sante/explor/ChloroquineV1/Data/Pmc/Corpus
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 0003580 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Pmc/Corpus/biblio.hfd -nk 0003580 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Sante
|area= ChloroquineV1
|flux= Pmc
|étape= Corpus
|type= RBID
|clé=
|texte=
}}
| This area was generated with Dilib version V0.6.33. |  |