Anticancer effect of SZC015 on lung cancer cells through ROS-dependent apoptosis and autophagy induction mechanisms in vitro.
Identifieur interne : 000D79 ( Main/Exploration ); précédent : 000D78; suivant : 000D80Anticancer effect of SZC015 on lung cancer cells through ROS-dependent apoptosis and autophagy induction mechanisms in vitro.
Auteurs : Bin Sun [République populaire de Chine] ; Lei Gao [République populaire de Chine] ; Anil Ahsan [République populaire de Chine] ; Peng Chu [République populaire de Chine] ; Yanlin Song [République populaire de Chine] ; Hailong Li [République populaire de Chine] ; Zonghui Zhang [République populaire de Chine] ; Yuan Lin [République populaire de Chine] ; Jinyong Peng [République populaire de Chine] ; Zhicheng Song [République populaire de Chine] ; Shisheng Wang [République populaire de Chine] ; Zeyao Tang [République populaire de Chine]Source :
- International immunopharmacology [ 1878-1705 ] ; 2016.
Descripteurs français
- KwdFr :
- Acide oléanolique (analogues et dérivés), Acide oléanolique (pharmacologie), Antinéoplasiques (pharmacologie), Apoptose (), Autophagie (), Espèces réactives de l'oxygène (métabolisme), Facteur de transcription NF-kappa B (métabolisme), Humains, Lignée cellulaire tumorale, Morpholines (pharmacologie), Points de contrôle du cycle cellulaire (), Protéine oncogène v-akt (métabolisme), Transduction du signal (), Tumeurs du poumon (anatomopathologie), Tumeurs du poumon (traitement médicamenteux).
- MESH :
- analogues et dérivés : Acide oléanolique.
- anatomopathologie : Tumeurs du poumon.
- métabolisme : Espèces réactives de l'oxygène, Facteur de transcription NF-kappa B, Protéine oncogène v-akt.
- pharmacologie : Acide oléanolique, Antinéoplasiques, Morpholines.
- traitement médicamenteux : Tumeurs du poumon.
- Apoptose, Autophagie, Humains, Lignée cellulaire tumorale, Points de contrôle du cycle cellulaire, Transduction du signal.
English descriptors
- KwdEn :
- Antineoplastic Agents (pharmacology), Apoptosis (drug effects), Autophagy (drug effects), Cell Cycle Checkpoints (drug effects), Cell Line, Tumor, Humans, Lung Neoplasms (drug therapy), Lung Neoplasms (pathology), Morpholines (pharmacology), NF-kappa B (metabolism), Oleanolic Acid (analogs & derivatives), Oleanolic Acid (pharmacology), Oncogene Protein v-akt (metabolism), Reactive Oxygen Species (metabolism), Signal Transduction (drug effects).
- MESH :
- chemical , analogs & derivatives : Oleanolic Acid.
- chemical , metabolism : NF-kappa B, Oncogene Protein v-akt, Reactive Oxygen Species.
- chemical , pharmacology : Antineoplastic Agents, Morpholines, Oleanolic Acid.
- drug effects : Apoptosis, Autophagy, Cell Cycle Checkpoints, Signal Transduction.
- drug therapy : Lung Neoplasms.
- pathology : Lung Neoplasms.
- Cell Line, Tumor, Humans.
Abstract
Oleanolic acid (OA) and its several derivatives possess various pharmacological activities, such as antitumor and anti-inflammation. In present study, anticancer effect of SZC015, an OA derivative, and its underlying mechanisms were investigated. We demonstrated that cell viability was significantly decreased in SZC015-treated lung cancer cells, but has less cytotoxicity in human bronchial epithelial cell line. Further investigation verified that apoptosis and autophagy induction and G0/G1 phase arrest were observed in SZC015-treated H322 cells. Mechanically, the level of Akt, p-Akt, p-IκBα, and total p65, the p-p65 in the cytoplasm and nucleus were suppressed by SZC015 in H322 cells, respectively. Inhibition of p65 nuclear translocation was also confirmed by immunofluorescence staining. In addition, co-treatment with chloroquine, an autophagy inhibitor, significantly inhibited SZC015-induced autophagy and enhanced SZC015-induced apoptotic cell death. Intracellular ROS was increased in a concentration-dependent manner, which could be prevented by N-Acetyl l-Cysteine, an ROS scavenger. Moreover, the level of Akt and procaspase-3 were increased, while the ratio of LC3 II/I was decreased. Taken together, our study demonstrates that the inhibitory effect of SZC015 against H322 cells is mediated by excessive ROS generation that could suppress Akt/NF-κB signaling pathway, which thereby leads to apoptotic and autophagic cell death.
DOI: 10.1016/j.intimp.2016.09.026
PubMed: 27697723
Affiliations:
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Department, Dalian Medical University, 9 West Section, South Road of Lvshun, Dalian</wicri:regionArea><wicri:noRegion>Dalian</wicri:noRegion></affiliation></author><author><name sortKey="Chu, Peng" sort="Chu, Peng" uniqKey="Chu P" first="Peng" last="Chu">Peng Chu</name><affiliation wicri:level="1"><nlm:affiliation>Pharmacology Department, Dalian Medical University, 9 West Section, South Road of Lvshun, Dalian, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Pharmacology Department, Dalian Medical University, 9 West Section, South Road of Lvshun, Dalian</wicri:regionArea><wicri:noRegion>Dalian</wicri:noRegion></affiliation></author><author><name sortKey="Song, Yanlin" sort="Song, Yanlin" uniqKey="Song Y" first="Yanlin" last="Song">Yanlin Song</name><affiliation wicri:level="1"><nlm:affiliation>Pharmacology Department, Dalian Medical University, 9 West Section, South Road of Lvshun, Dalian, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Pharmacology Department, Dalian Medical University, 9 West Section, South Road of Lvshun, Dalian</wicri:regionArea><wicri:noRegion>Dalian</wicri:noRegion></affiliation></author><author><name sortKey="Li, Hailong" sort="Li, Hailong" uniqKey="Li H" first="Hailong" last="Li">Hailong Li</name><affiliation wicri:level="1"><nlm:affiliation>Pharmacology Department, Dalian Medical University, 9 West Section, South Road of Lvshun, Dalian, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Pharmacology Department, Dalian Medical University, 9 West Section, South Road of Lvshun, Dalian</wicri:regionArea><wicri:noRegion>Dalian</wicri:noRegion></affiliation></author><author><name sortKey="Zhang, Zonghui" sort="Zhang, Zonghui" uniqKey="Zhang Z" first="Zonghui" last="Zhang">Zonghui Zhang</name><affiliation wicri:level="1"><nlm:affiliation>Pharmacology Department, Dalian Medical University, 9 West Section, South Road of Lvshun, Dalian, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Pharmacology Department, Dalian Medical University, 9 West Section, South Road of Lvshun, Dalian</wicri:regionArea><wicri:noRegion>Dalian</wicri:noRegion></affiliation></author><author><name sortKey="Lin, Yuan" sort="Lin, Yuan" uniqKey="Lin Y" first="Yuan" last="Lin">Yuan Lin</name><affiliation wicri:level="1"><nlm:affiliation>Pharmacology Department, Dalian Medical University, 9 West Section, South Road of Lvshun, Dalian, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Pharmacology Department, Dalian Medical University, 9 West Section, South Road of Lvshun, Dalian</wicri:regionArea><wicri:noRegion>Dalian</wicri:noRegion></affiliation></author><author><name sortKey="Peng, Jinyong" sort="Peng, Jinyong" uniqKey="Peng J" first="Jinyong" last="Peng">Jinyong Peng</name><affiliation wicri:level="1"><nlm:affiliation>Pharmacology Department, Dalian Medical University, 9 West Section, South Road of Lvshun, Dalian, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Pharmacology Department, Dalian Medical University, 9 West Section, South Road of Lvshun, Dalian</wicri:regionArea><wicri:noRegion>Dalian</wicri:noRegion></affiliation></author><author><name sortKey="Song, Zhicheng" sort="Song, Zhicheng" uniqKey="Song Z" first="Zhicheng" last="Song">Zhicheng Song</name><affiliation wicri:level="1"><nlm:affiliation>College of Pharmaceutical Science and Technology, Dalian University of Technology, Dalian, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>College of Pharmaceutical Science and Technology, Dalian University of Technology, Dalian</wicri:regionArea><wicri:noRegion>Dalian</wicri:noRegion></affiliation></author><author><name sortKey="Wang, Shisheng" sort="Wang, Shisheng" uniqKey="Wang S" first="Shisheng" last="Wang">Shisheng Wang</name><affiliation wicri:level="1"><nlm:affiliation>College of Pharmaceutical Science and Technology, Dalian University of Technology, Dalian, China. Electronic address: wangss@dlut.edu.cn.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>College of Pharmaceutical Science and Technology, Dalian University of Technology, Dalian</wicri:regionArea><wicri:noRegion>Dalian</wicri:noRegion></affiliation></author><author><name sortKey="Tang, Zeyao" sort="Tang, Zeyao" uniqKey="Tang Z" first="Zeyao" last="Tang">Zeyao Tang</name><affiliation wicri:level="1"><nlm:affiliation>Pharmacology Department, Dalian Medical University, 9 West Section, South Road of Lvshun, Dalian, China. Electronic address: tangzeyao@aliyun.com.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Pharmacology Department, Dalian Medical University, 9 West Section, South Road of Lvshun, Dalian</wicri:regionArea><wicri:noRegion>Dalian</wicri:noRegion></affiliation></author></analytic><series><title level="j">International immunopharmacology</title><idno type="eISSN">1878-1705</idno><imprint><date when="2016" type="published">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Antineoplastic Agents (pharmacology)</term><term>Apoptosis (drug effects)</term><term>Autophagy (drug effects)</term><term>Cell Cycle Checkpoints (drug effects)</term><term>Cell Line, Tumor</term><term>Humans</term><term>Lung Neoplasms (drug therapy)</term><term>Lung Neoplasms (pathology)</term><term>Morpholines (pharmacology)</term><term>NF-kappa B (metabolism)</term><term>Oleanolic Acid (analogs & derivatives)</term><term>Oleanolic Acid (pharmacology)</term><term>Oncogene Protein v-akt (metabolism)</term><term>Reactive Oxygen Species (metabolism)</term><term>Signal Transduction (drug effects)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Acide oléanolique (analogues et dérivés)</term><term>Acide oléanolique (pharmacologie)</term><term>Antinéoplasiques (pharmacologie)</term><term>Apoptose ()</term><term>Autophagie ()</term><term>Espèces réactives de l'oxygène (métabolisme)</term><term>Facteur de transcription NF-kappa B (métabolisme)</term><term>Humains</term><term>Lignée cellulaire tumorale</term><term>Morpholines (pharmacologie)</term><term>Points de contrôle du cycle cellulaire ()</term><term>Protéine oncogène v-akt (métabolisme)</term><term>Transduction du signal ()</term><term>Tumeurs du poumon (anatomopathologie)</term><term>Tumeurs du poumon (traitement médicamenteux)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analogs & derivatives" xml:lang="en"><term>Oleanolic Acid</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>NF-kappa B</term><term>Oncogene Protein v-akt</term><term>Reactive Oxygen Species</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Antineoplastic Agents</term><term>Morpholines</term><term>Oleanolic Acid</term></keywords><keywords scheme="MESH" qualifier="analogues et dérivés" xml:lang="fr"><term>Acide oléanolique</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Tumeurs du poumon</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Apoptosis</term><term>Autophagy</term><term>Cell Cycle Checkpoints</term><term>Signal Transduction</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Lung Neoplasms</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Espèces réactives de l'oxygène</term><term>Facteur de transcription NF-kappa B</term><term>Protéine oncogène v-akt</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Lung Neoplasms</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Acide oléanolique</term><term>Antinéoplasiques</term><term>Morpholines</term></keywords><keywords scheme="MESH" qualifier="traitement médicamenteux" xml:lang="fr"><term>Tumeurs du poumon</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Cell Line, Tumor</term><term>Humans</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Apoptose</term><term>Autophagie</term><term>Humains</term><term>Lignée cellulaire tumorale</term><term>Points de contrôle du cycle cellulaire</term><term>Transduction du signal</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Oleanolic acid (OA) and its several derivatives possess various pharmacological activities, such as antitumor and anti-inflammation. In present study, anticancer effect of SZC015, an OA derivative, and its underlying mechanisms were investigated. We demonstrated that cell viability was significantly decreased in SZC015-treated lung cancer cells, but has less cytotoxicity in human bronchial epithelial cell line. Further investigation verified that apoptosis and autophagy induction and G<sub>0</sub>/G<sub>1</sub> phase arrest were observed in SZC015-treated H322 cells. Mechanically, the level of Akt, p-Akt, p-IκBα, and total p65, the p-p65 in the cytoplasm and nucleus were suppressed by SZC015 in H322 cells, respectively. Inhibition of p65 nuclear translocation was also confirmed by immunofluorescence staining. In addition, co-treatment with chloroquine, an autophagy inhibitor, significantly inhibited SZC015-induced autophagy and enhanced SZC015-induced apoptotic cell death. Intracellular ROS was increased in a concentration-dependent manner, which could be prevented by N-Acetyl l-Cysteine, an ROS scavenger. Moreover, the level of Akt and procaspase-3 were increased, while the ratio of LC3 II/I was decreased. Taken together, our study demonstrates that the inhibitory effect of SZC015 against H322 cells is mediated by excessive ROS generation that could suppress Akt/NF-κB signaling pathway, which thereby leads to apoptotic and autophagic cell death.</div></front></TEI><affiliations><list><country><li>République populaire de Chine</li></country></list><tree><country name="République populaire de Chine"><noRegion><name sortKey="Sun, Bin" sort="Sun, Bin" uniqKey="Sun B" first="Bin" last="Sun">Bin Sun</name></noRegion><name sortKey="Ahsan, Anil" sort="Ahsan, Anil" uniqKey="Ahsan A" first="Anil" last="Ahsan">Anil Ahsan</name><name sortKey="Chu, Peng" sort="Chu, Peng" uniqKey="Chu P" first="Peng" last="Chu">Peng Chu</name><name sortKey="Gao, Lei" sort="Gao, Lei" uniqKey="Gao L" first="Lei" last="Gao">Lei Gao</name><name sortKey="Li, Hailong" sort="Li, Hailong" uniqKey="Li H" first="Hailong" last="Li">Hailong Li</name><name sortKey="Lin, Yuan" sort="Lin, Yuan" uniqKey="Lin Y" first="Yuan" last="Lin">Yuan Lin</name><name sortKey="Peng, Jinyong" sort="Peng, Jinyong" uniqKey="Peng J" first="Jinyong" last="Peng">Jinyong Peng</name><name sortKey="Song, Yanlin" sort="Song, Yanlin" uniqKey="Song Y" first="Yanlin" last="Song">Yanlin Song</name><name sortKey="Song, Zhicheng" sort="Song, Zhicheng" uniqKey="Song Z" first="Zhicheng" last="Song">Zhicheng Song</name><name sortKey="Tang, Zeyao" sort="Tang, Zeyao" uniqKey="Tang Z" first="Zeyao" last="Tang">Zeyao Tang</name><name sortKey="Wang, Shisheng" sort="Wang, Shisheng" uniqKey="Wang S" first="Shisheng" last="Wang">Shisheng Wang</name><name sortKey="Zhang, Zonghui" sort="Zhang, Zonghui" uniqKey="Zhang Z" first="Zonghui" last="Zhang">Zonghui Zhang</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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HfdIndexSelect -h $EXPLOR_AREA/Data/Main/Exploration/RBID.i -Sk "pubmed:27697723" \
| HfdSelect -Kh $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd \
| NlmPubMed2Wicri -a ChloroquineV1
| This area was generated with Dilib version V0.6.33. |  |