Mimulone-induced autophagy through p53-mediated AMPK/mTOR pathway increases caspase-mediated apoptotic cell death in A549 human lung cancer cells.
Identifieur interne : 001014 ( Main/Exploration ); précédent : 001013; suivant : 001015Mimulone-induced autophagy through p53-mediated AMPK/mTOR pathway increases caspase-mediated apoptotic cell death in A549 human lung cancer cells.
Auteurs : Hyun-Kyu An [Corée du Sud] ; Kyoung-Sook Kim [Corée du Sud] ; Ji-Won Lee [Corée du Sud] ; Mi-Hyun Park [Corée du Sud] ; Hyung-In Moon [Corée du Sud] ; Shin-Ji Park [Corée du Sud] ; Ji-Sue Baik [Corée du Sud] ; Cheorl-Ho Kim [Corée du Sud] ; Young-Choon Lee [Corée du Sud]Source :
- PloS one [ 1932-6203 ] ; 2014.
Descripteurs français
- KwdFr :
- AMP-Activated Protein Kinases (métabolisme), Adénocarcinome (anatomopathologie), Antinéoplasiques d'origine végétale (pharmacologie), Apoptose (), Autophagie (), Benzothiazoles, Cellules HCT116, Cellules MCF-7, Flavanones (pharmacologie), Humains, Lamiales (), Lignée cellulaire tumorale, Protéine p53 suppresseur de tumeur (génétique), Protéine p53 suppresseur de tumeur (métabolisme), Survie cellulaire (), Sérine-thréonine kinases TOR (métabolisme), Techniques de knock-down de gènes, Toluène (analogues et dérivés), Tumeurs du poumon (anatomopathologie).
- MESH :
- analogues et dérivés : Toluène.
- anatomopathologie : Adénocarcinome, Tumeurs du poumon.
- génétique : Protéine p53 suppresseur de tumeur.
- métabolisme : AMP-Activated Protein Kinases, Protéine p53 suppresseur de tumeur, Sérine-thréonine kinases TOR.
- pharmacologie : Antinéoplasiques d'origine végétale, Flavanones.
- Apoptose, Autophagie, Benzothiazoles, Cellules HCT116, Cellules MCF-7, Humains, Lamiales, Lignée cellulaire tumorale, Survie cellulaire, Techniques de knock-down de gènes.
English descriptors
- KwdEn :
- AMP-Activated Protein Kinases (metabolism), Adenocarcinoma (pathology), Adenocarcinoma of Lung, Antineoplastic Agents, Phytogenic (pharmacology), Apoptosis (drug effects), Autophagy (drug effects), Benzothiazoles, Cell Line, Tumor, Cell Survival (drug effects), Flavanones (pharmacology), Gene Knockdown Techniques, HCT116 Cells, Humans, Lamiales (chemistry), Lung Neoplasms (pathology), MCF-7 Cells, TOR Serine-Threonine Kinases (metabolism), Toluene (analogs & derivatives), Tumor Suppressor Protein p53 (genetics), Tumor Suppressor Protein p53 (metabolism).
- MESH :
- chemical , analogs & derivatives : Toluene.
- chemical , genetics : Tumor Suppressor Protein p53.
- chemical , metabolism : AMP-Activated Protein Kinases, TOR Serine-Threonine Kinases, Tumor Suppressor Protein p53.
- chemistry : Lamiales.
- drug effects : Apoptosis, Autophagy, Cell Survival.
- pathology : Adenocarcinoma, Lung Neoplasms.
- chemical , pharmacology : Antineoplastic Agents, Phytogenic, Flavanones.
- Adenocarcinoma of Lung, Benzothiazoles, Cell Line, Tumor, Gene Knockdown Techniques, HCT116 Cells, Humans, MCF-7 Cells.
Abstract
Anticancer properties and mechanisms of mimulone (MML), C-geranylflavonoid isolated from the Paulownia tomentosa fruits, were firstly elucidated in this study. MML prevented cell proliferation in a dose- and time-dependent way and triggered apoptosis through the extrinsic pathway in A549 human lung adenocarcinoma cells. Furthermore, MML-treated cells displayed autophagic features, such as the formation of autophagic vacuoles, a primary morphological feature of autophagy, and the accumulation of microtubule-associated protein 1 light chain 3 (LC3) puncta, another typical maker of autophagy, as determined by FITC-conjugated immunostaining and monodansylcadaverine (MDC) staining, respectively. The expression levels of LC3-I and LC3-II, specific markers of autophagy, were also augmented by MML treatment. Autophagy inhibition by 3-methyladenine (3-MA), pharmacological autophagy inhibitor, and shRNA knockdown of Beclin-1 reduced apoptotic cell death induced by MML. Autophagic flux was not significantly affected by MML treatment and lysosomal inhibitor, chloroquine (CQ) suppressed MML-induced autophagy and apoptosis. MML-induced autophagy was promoted by decreases in p53 and p-mTOR levels and increase of p-AMPK. Moreover, inhibition of p53 transactivation by pifithrin-α (PFT-α) and knockdown of p53 enhanced induction of autophagy and finally promoted apoptotic cell death. Overall, the results demonstrate that autophagy contributes to the cytotoxicity of MML in cancer cells harboring wild-type p53. This study strongly suggests that MML is a potential candidate for an anticancer agent targeting both autophagy and apoptotic cell death in human lung cancer. Moreover, co-treatment of MML and p53 inhibitor would be more effective in human lung cancer therapy.
DOI: 10.1371/journal.pone.0114607
PubMed: 25490748
Affiliations:
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pathway increases caspase-mediated apoptotic cell death in A549 human lung cancer cells.</title><author><name sortKey="An, Hyun Kyu" sort="An, Hyun Kyu" uniqKey="An H" first="Hyun-Kyu" last="An">Hyun-Kyu An</name><affiliation wicri:level="1"><nlm:affiliation>College of Natural Resources and Life Science, Dong-A University, Busan, 604-714, South Korea.</nlm:affiliation><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>College of Natural Resources and Life Science, Dong-A University, Busan, 604-714</wicri:regionArea><wicri:noRegion>604-714</wicri:noRegion></affiliation></author><author><name sortKey="Kim, Kyoung Sook" sort="Kim, Kyoung Sook" uniqKey="Kim K" first="Kyoung-Sook" last="Kim">Kyoung-Sook Kim</name><affiliation wicri:level="1"><nlm:affiliation>College of Natural Resources and Life Science, Dong-A University, Busan, 604-714, South Korea.</nlm:affiliation><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>College of Natural Resources and Life Science, Dong-A University, Busan, 604-714</wicri:regionArea><wicri:noRegion>604-714</wicri:noRegion></affiliation></author><author><name sortKey="Lee, Ji Won" sort="Lee, Ji Won" uniqKey="Lee J" first="Ji-Won" last="Lee">Ji-Won Lee</name><affiliation wicri:level="1"><nlm:affiliation>College of Natural Resources and Life Science, Dong-A University, Busan, 604-714, South Korea.</nlm:affiliation><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>College of Natural Resources and Life Science, Dong-A University, Busan, 604-714</wicri:regionArea><wicri:noRegion>604-714</wicri:noRegion></affiliation></author><author><name sortKey="Park, Mi Hyun" sort="Park, Mi Hyun" uniqKey="Park M" first="Mi-Hyun" last="Park">Mi-Hyun Park</name><affiliation wicri:level="1"><nlm:affiliation>College of Natural Resources and Life Science, Dong-A University, Busan, 604-714, South Korea.</nlm:affiliation><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>College of Natural Resources and Life 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Resources and Life Science, Dong-A University, Busan, 604-714</wicri:regionArea><wicri:noRegion>604-714</wicri:noRegion></affiliation></author><author><name sortKey="Baik, Ji Sue" sort="Baik, Ji Sue" uniqKey="Baik J" first="Ji-Sue" last="Baik">Ji-Sue Baik</name><affiliation wicri:level="1"><nlm:affiliation>College of Natural Resources and Life Science, Dong-A University, Busan, 604-714, South Korea.</nlm:affiliation><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>College of Natural Resources and Life Science, Dong-A University, Busan, 604-714</wicri:regionArea><wicri:noRegion>604-714</wicri:noRegion></affiliation></author><author><name sortKey="Kim, Cheorl Ho" sort="Kim, Cheorl Ho" uniqKey="Kim C" first="Cheorl-Ho" last="Kim">Cheorl-Ho Kim</name><affiliation wicri:level="1"><nlm:affiliation>Molecular and Cellular Glycobiology Unit, Department of Biological Sciences, SungKyunKwan University, Kyunggi-Do, 440-746, South Korea.</nlm:affiliation><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Molecular and Cellular Glycobiology Unit, Department of Biological Sciences, SungKyunKwan University, Kyunggi-Do, 440-746</wicri:regionArea><wicri:noRegion>440-746</wicri:noRegion></affiliation></author><author><name sortKey="Lee, Young Choon" sort="Lee, Young Choon" uniqKey="Lee Y" first="Young-Choon" last="Lee">Young-Choon Lee</name><affiliation wicri:level="1"><nlm:affiliation>College of Natural Resources and Life Science, Dong-A University, Busan, 604-714, South Korea.</nlm:affiliation><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>College of Natural Resources and Life Science, Dong-A University, Busan, 604-714</wicri:regionArea><wicri:noRegion>604-714</wicri:noRegion></affiliation></author></analytic><series><title level="j">PloS one</title><idno type="eISSN">1932-6203</idno><imprint><date when="2014" type="published">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>AMP-Activated Protein Kinases (metabolism)</term><term>Adenocarcinoma (pathology)</term><term>Adenocarcinoma of Lung</term><term>Antineoplastic Agents, Phytogenic (pharmacology)</term><term>Apoptosis (drug effects)</term><term>Autophagy (drug effects)</term><term>Benzothiazoles</term><term>Cell Line, Tumor</term><term>Cell Survival (drug effects)</term><term>Flavanones (pharmacology)</term><term>Gene Knockdown Techniques</term><term>HCT116 Cells</term><term>Humans</term><term>Lamiales (chemistry)</term><term>Lung Neoplasms (pathology)</term><term>MCF-7 Cells</term><term>TOR Serine-Threonine Kinases (metabolism)</term><term>Toluene (analogs & derivatives)</term><term>Tumor Suppressor Protein p53 (genetics)</term><term>Tumor Suppressor Protein p53 (metabolism)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>AMP-Activated Protein Kinases (métabolisme)</term><term>Adénocarcinome (anatomopathologie)</term><term>Antinéoplasiques d'origine végétale (pharmacologie)</term><term>Apoptose ()</term><term>Autophagie ()</term><term>Benzothiazoles</term><term>Cellules HCT116</term><term>Cellules MCF-7</term><term>Flavanones (pharmacologie)</term><term>Humains</term><term>Lamiales ()</term><term>Lignée cellulaire tumorale</term><term>Protéine p53 suppresseur de tumeur (génétique)</term><term>Protéine p53 suppresseur de tumeur (métabolisme)</term><term>Survie cellulaire ()</term><term>Sérine-thréonine kinases TOR (métabolisme)</term><term>Techniques de knock-down de gènes</term><term>Toluène (analogues et dérivés)</term><term>Tumeurs du poumon (anatomopathologie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analogs & derivatives" xml:lang="en"><term>Toluene</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Tumor Suppressor Protein p53</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>AMP-Activated Protein Kinases</term><term>TOR Serine-Threonine Kinases</term><term>Tumor Suppressor Protein p53</term></keywords><keywords scheme="MESH" qualifier="analogues et dérivés" xml:lang="fr"><term>Toluène</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Adénocarcinome</term><term>Tumeurs du poumon</term></keywords><keywords scheme="MESH" qualifier="chemistry" xml:lang="en"><term>Lamiales</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Apoptosis</term><term>Autophagy</term><term>Cell Survival</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Protéine p53 suppresseur de tumeur</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>AMP-Activated Protein Kinases</term><term>Protéine p53 suppresseur de tumeur</term><term>Sérine-thréonine kinases TOR</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Adenocarcinoma</term><term>Lung Neoplasms</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Antinéoplasiques d'origine végétale</term><term>Flavanones</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Antineoplastic Agents, Phytogenic</term><term>Flavanones</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adenocarcinoma of Lung</term><term>Benzothiazoles</term><term>Cell Line, Tumor</term><term>Gene Knockdown Techniques</term><term>HCT116 Cells</term><term>Humans</term><term>MCF-7 Cells</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Apoptose</term><term>Autophagie</term><term>Benzothiazoles</term><term>Cellules HCT116</term><term>Cellules MCF-7</term><term>Humains</term><term>Lamiales</term><term>Lignée cellulaire tumorale</term><term>Survie cellulaire</term><term>Techniques de knock-down de gènes</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Anticancer properties and mechanisms of mimulone (MML), C-geranylflavonoid isolated from the Paulownia tomentosa fruits, were firstly elucidated in this study. MML prevented cell proliferation in a dose- and time-dependent way and triggered apoptosis through the extrinsic pathway in A549 human lung adenocarcinoma cells. Furthermore, MML-treated cells displayed autophagic features, such as the formation of autophagic vacuoles, a primary morphological feature of autophagy, and the accumulation of microtubule-associated protein 1 light chain 3 (LC3) puncta, another typical maker of autophagy, as determined by FITC-conjugated immunostaining and monodansylcadaverine (MDC) staining, respectively. The expression levels of LC3-I and LC3-II, specific markers of autophagy, were also augmented by MML treatment. Autophagy inhibition by 3-methyladenine (3-MA), pharmacological autophagy inhibitor, and shRNA knockdown of Beclin-1 reduced apoptotic cell death induced by MML. Autophagic flux was not significantly affected by MML treatment and lysosomal inhibitor, chloroquine (CQ) suppressed MML-induced autophagy and apoptosis. MML-induced autophagy was promoted by decreases in p53 and p-mTOR levels and increase of p-AMPK. Moreover, inhibition of p53 transactivation by pifithrin-α (PFT-α) and knockdown of p53 enhanced induction of autophagy and finally promoted apoptotic cell death. Overall, the results demonstrate that autophagy contributes to the cytotoxicity of MML in cancer cells harboring wild-type p53. This study strongly suggests that MML is a potential candidate for an anticancer agent targeting both autophagy and apoptotic cell death in human lung cancer. Moreover, co-treatment of MML and p53 inhibitor would be more effective in human lung cancer therapy. </div></front></TEI><affiliations><list><country><li>Corée du Sud</li></country></list><tree><country name="Corée du Sud"><noRegion><name sortKey="An, Hyun Kyu" sort="An, Hyun Kyu" uniqKey="An H" first="Hyun-Kyu" last="An">Hyun-Kyu An</name></noRegion><name sortKey="Baik, Ji Sue" sort="Baik, Ji Sue" uniqKey="Baik J" first="Ji-Sue" last="Baik">Ji-Sue Baik</name><name sortKey="Kim, Cheorl Ho" sort="Kim, Cheorl Ho" uniqKey="Kim C" first="Cheorl-Ho" last="Kim">Cheorl-Ho Kim</name><name sortKey="Kim, Kyoung Sook" sort="Kim, Kyoung Sook" uniqKey="Kim K" first="Kyoung-Sook" last="Kim">Kyoung-Sook Kim</name><name sortKey="Lee, Ji Won" sort="Lee, Ji Won" uniqKey="Lee J" first="Ji-Won" last="Lee">Ji-Won Lee</name><name sortKey="Lee, Young Choon" sort="Lee, Young Choon" uniqKey="Lee Y" first="Young-Choon" last="Lee">Young-Choon Lee</name><name sortKey="Moon, Hyung In" sort="Moon, Hyung In" uniqKey="Moon H" first="Hyung-In" last="Moon">Hyung-In Moon</name><name sortKey="Park, Mi Hyun" sort="Park, Mi Hyun" uniqKey="Park M" first="Mi-Hyun" last="Park">Mi-Hyun Park</name><name sortKey="Park, Shin Ji" sort="Park, Shin Ji" uniqKey="Park S" first="Shin-Ji" last="Park">Shin-Ji Park</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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