Licarin A induces cell death by activation of autophagy and apoptosis in non-small cell lung cancer cells.
Identifieur interne : 000C27 ( Main/Exploration ); précédent : 000C26; suivant : 000C28Licarin A induces cell death by activation of autophagy and apoptosis in non-small cell lung cancer cells.
Auteurs : Uma Maheswari [Inde] ; Krishna Ghosh [Inde] ; Sudha Rani Sadras [Inde]Source :
- Apoptosis : an international journal on programmed cell death [ 1573-675X ] ; 2018.
Descripteurs français
- KwdFr :
- Antinéoplasiques d'origine végétale (pharmacologie), Apoptose (), Autophagie (), Bécline-1 (génétique), Bécline-1 (métabolisme), Carcinome pulmonaire non à petites cellules (génétique), Carcinome pulmonaire non à petites cellules (métabolisme), Carcinome pulmonaire non à petites cellules (physiopathologie), Carcinome pulmonaire non à petites cellules (traitement médicamenteux), Caspase-3 (génétique), Caspase-3 (métabolisme), Cellules A549, Espèces réactives de l'oxygène (métabolisme), Extraits de plantes (pharmacologie), Humains, Lignanes (pharmacologie), Récepteurs activés par les proliférateurs de peroxysomes (génétique), Récepteurs activés par les proliférateurs de peroxysomes (métabolisme), Tumeurs du poumon (génétique), Tumeurs du poumon (métabolisme), Tumeurs du poumon (physiopathologie).
- MESH :
- génétique : Bécline-1, Carcinome pulmonaire non à petites cellules, Caspase-3, Récepteurs activés par les proliférateurs de peroxysomes, Tumeurs du poumon.
- métabolisme : Bécline-1, Carcinome pulmonaire non à petites cellules, Caspase-3, Espèces réactives de l'oxygène, Récepteurs activés par les proliférateurs de peroxysomes, Tumeurs du poumon.
- pharmacologie : Antinéoplasiques d'origine végétale, Extraits de plantes, Lignanes.
- physiopathologie : Carcinome pulmonaire non à petites cellules, Tumeurs du poumon.
- traitement médicamenteux : Carcinome pulmonaire non à petites cellules.
- Apoptose, Autophagie, Cellules A549, Humains.
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
Affiliations:
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Le document en format XML
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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 wicri:level="1"><nlm:affiliation>DBT-IPLS Programme, Department of Biochemistry and Molecular Biology, Pondicherry University, Pondicherry, 605014, India.</nlm:affiliation><country xml:lang="fr">Inde</country><wicri:regionArea>DBT-IPLS Programme, Department of Biochemistry and Molecular Biology, Pondicherry University, Pondicherry, 605014</wicri:regionArea><wicri:noRegion>605014</wicri:noRegion></affiliation></author><author><name sortKey="Ghosh, Krishna" sort="Ghosh, Krishna" uniqKey="Ghosh K" first="Krishna" last="Ghosh">Krishna Ghosh</name><affiliation wicri:level="1"><nlm:affiliation>Department of Biochemistry and Molecular Biology, Central University of Kerala, Kasaragod, Kerala, 671314, India.</nlm:affiliation><country xml:lang="fr">Inde</country><wicri:regionArea>Department of Biochemistry and Molecular Biology, Central University of Kerala, Kasaragod, Kerala, 671314</wicri:regionArea><wicri:noRegion>671314</wicri:noRegion></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 wicri:level="1"><nlm:affiliation>DBT-IPLS Programme, Department of Biochemistry and Molecular Biology, Pondicherry University, Pondicherry, 605014, India. dr.ssrlab@gmail.com.</nlm:affiliation><country xml:lang="fr">Inde</country><wicri:regionArea>DBT-IPLS Programme, Department of Biochemistry and Molecular Biology, Pondicherry University, Pondicherry, 605014</wicri:regionArea><wicri:noRegion>605014</wicri:noRegion></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" 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(metabolism)</term><term>Plant Extracts (pharmacology)</term><term>Reactive Oxygen Species (metabolism)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Antinéoplasiques d'origine végétale (pharmacologie)</term><term>Apoptose ()</term><term>Autophagie ()</term><term>Bécline-1 (génétique)</term><term>Bécline-1 (métabolisme)</term><term>Carcinome pulmonaire non à petites cellules (génétique)</term><term>Carcinome pulmonaire non à petites cellules (métabolisme)</term><term>Carcinome pulmonaire non à petites cellules (physiopathologie)</term><term>Carcinome pulmonaire non à petites cellules (traitement médicamenteux)</term><term>Caspase-3 (génétique)</term><term>Caspase-3 (métabolisme)</term><term>Cellules A549</term><term>Espèces réactives de l'oxygène (métabolisme)</term><term>Extraits de plantes (pharmacologie)</term><term>Humains</term><term>Lignanes (pharmacologie)</term><term>Récepteurs activés par les proliférateurs de peroxysomes (génétique)</term><term>Récepteurs 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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="génétique" xml:lang="fr"><term>Bécline-1</term><term>Carcinome pulmonaire non à petites cellules</term><term>Caspase-3</term><term>Récepteurs activés par les proliférateurs de peroxysomes</term><term>Tumeurs du poumon</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="métabolisme" xml:lang="fr"><term>Bécline-1</term><term>Carcinome pulmonaire non à petites cellules</term><term>Caspase-3</term><term>Espèces réactives de l'oxygène</term><term>Récepteurs activés par les proliférateurs de 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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><affiliations><list><country><li>Inde</li></country></list><tree><country name="Inde"><noRegion><name sortKey="Maheswari, Uma" sort="Maheswari, Uma" uniqKey="Maheswari U" first="Uma" last="Maheswari">Uma Maheswari</name></noRegion><name sortKey="Ghosh, Krishna" sort="Ghosh, Krishna" uniqKey="Ghosh K" first="Krishna" last="Ghosh">Krishna Ghosh</name><name sortKey="Sadras, Sudha Rani" sort="Sadras, Sudha Rani" uniqKey="Sadras S" first="Sudha Rani" last="Sadras">Sudha Rani Sadras</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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