Induction of reactive oxygen species-stimulated distinctive autophagy by chelerythrine in non-small cell lung cancer cells.
Identifieur interne : 000D12 ( Main/Exploration ); précédent : 000D11; suivant : 000D13Induction of reactive oxygen species-stimulated distinctive autophagy by chelerythrine in non-small cell lung cancer cells.
Auteurs : Zheng-Hai Tang [République populaire de Chine] ; Wen-Xiang Cao [République populaire de Chine] ; Zhao-Yu Wang [République populaire de Chine] ; Jia-Hong Lu [République populaire de Chine] ; Bo Liu [République populaire de Chine] ; Xiuping Chen [République populaire de Chine] ; Jin-Jian Lu [République populaire de Chine]Source :
- Redox biology [ 2213-2317 ] ; 2017.
Descripteurs français
- KwdFr :
- Antinéoplasiques (pharmacologie), Autophagie, Benzophénanthridines (pharmacologie), Carcinome pulmonaire non à petites cellules (métabolisme), Cellules A549, Espèces réactives de l'oxygène (métabolisme), Humains, Lignée cellulaire tumorale, Prolifération cellulaire (), Protéines associées aux microtubules (métabolisme), Relation dose-effet des médicaments, Régulation de l'expression des gènes tumoraux (), Survie cellulaire (), Tumeurs du poumon (métabolisme).
- MESH :
- métabolisme : Carcinome pulmonaire non à petites cellules, Espèces réactives de l'oxygène, Protéines associées aux microtubules, Tumeurs du poumon.
- pharmacologie : Antinéoplasiques, Benzophénanthridines.
- Autophagie, Cellules A549, Humains, Lignée cellulaire tumorale, Prolifération cellulaire, Relation dose-effet des médicaments, Régulation de l'expression des gènes tumoraux, Survie cellulaire.
English descriptors
- KwdEn :
- A549 Cells, Antineoplastic Agents (pharmacology), Autophagy, Benzophenanthridines (pharmacology), Carcinoma, Non-Small-Cell Lung (metabolism), Cell Line, Tumor, Cell Proliferation (drug effects), Cell Survival (drug effects), Dose-Response Relationship, Drug, Gene Expression Regulation, Neoplastic (drug effects), Humans, Lung Neoplasms (metabolism), Microtubule-Associated Proteins (metabolism), Reactive Oxygen Species (metabolism).
- MESH :
- chemical , metabolism : Microtubule-Associated Proteins, Reactive Oxygen Species.
- chemical , pharmacology : Antineoplastic Agents, Benzophenanthridines.
- drug effects : Cell Proliferation, Cell Survival, Gene Expression Regulation, Neoplastic.
- metabolism : Carcinoma, Non-Small-Cell Lung, Lung Neoplasms.
- A549 Cells, Autophagy, Cell Line, Tumor, Dose-Response Relationship, Drug, Humans.
Abstract
Chelerythrine (CHE), a natural benzo[c]phenanthridine alkaloid, shows anti-cancer effect through a number of mechanisms. Herein, the effect and mechanism of the CHE-induced autophagy, a type II programmed cell death, in non-small cell lung cancer (NSCLC) cells were studied for the first time. CHE induced cell viability decrease, colony formation inhibition, and apoptosis in a concentration-dependent manner in NSCLC A549 and NCI-H1299 cells. In addition, CHE triggered the expression of phosphatidylethanolamine-modified microtubule-associated protein light-chain 3 (LC3-II). The CHE-induced expression of LC3-II was further increased in the combination treatment with chloroquine (CQ), an autophagy inhibitor, and large amounts of red-puncta were observed in the CHE-treated A549 cells with stable expression of mRFP-EGFP-LC3, indicating that CHE induces autophagy flux. Silence of beclin 1 reversed the CHE-induced expression of LC3-II. Inhibition of autophagy remarkably reversed the CHE-induced cell viability decrease and apoptosis in NCI-H1299 cells but not in A549 cells. Furthermore, CHE triggered reactive oxygen species (ROS) generation in both cell lines. A decreased level of ROS through pretreatment with N-acetyl-L-cysteine reversed the CHE-induced cell viability decrease, apoptosis, and autophagy. Taken together, CHE induced distinctive autophagy in A549 (accompanied autophagy) and NCI-H1299 (pro-death autophagy) cells and a decreased level of ROS reversed the effect of CHE in NSCLC cells in terms of cell viability, apoptosis, and autophagy.
DOI: 10.1016/j.redox.2017.03.009
PubMed: 28288416
Affiliations:
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Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao</wicri:regionArea><wicri:noRegion>Macao</wicri:noRegion></affiliation></author><author><name sortKey="Cao, Wen Xiang" sort="Cao, Wen Xiang" uniqKey="Cao W" first="Wen-Xiang" last="Cao">Wen-Xiang Cao</name><affiliation wicri:level="1"><nlm:affiliation>State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao</wicri:regionArea><wicri:noRegion>Macao</wicri:noRegion></affiliation></author><author><name sortKey="Wang, Zhao Yu" sort="Wang, Zhao Yu" uniqKey="Wang Z" first="Zhao-Yu" last="Wang">Zhao-Yu Wang</name><affiliation wicri:level="1"><nlm:affiliation>State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao</wicri:regionArea><wicri:noRegion>Macao</wicri:noRegion></affiliation></author><author><name sortKey="Lu, Jia Hong" sort="Lu, Jia Hong" uniqKey="Lu J" first="Jia-Hong" last="Lu">Jia-Hong Lu</name><affiliation wicri:level="1"><nlm:affiliation>State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao</wicri:regionArea><wicri:noRegion>Macao</wicri:noRegion></affiliation></author><author><name sortKey="Liu, Bo" sort="Liu, Bo" uniqKey="Liu B" first="Bo" last="Liu">Bo Liu</name><affiliation wicri:level="3"><nlm:affiliation>The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangdong Provincial Academy of Chinese Medical Sciences, Guangzhou, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangdong Provincial Academy of Chinese Medical Sciences, Guangzhou</wicri:regionArea><placeName><settlement type="city">Jiangmen</settlement><region type="province">Guangdong</region></placeName></affiliation></author><author><name sortKey="Chen, Xiuping" sort="Chen, Xiuping" uniqKey="Chen X" first="Xiuping" last="Chen">Xiuping Chen</name><affiliation wicri:level="1"><nlm:affiliation>State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao</wicri:regionArea><wicri:noRegion>Macao</wicri:noRegion></affiliation></author><author><name sortKey="Lu, Jin Jian" sort="Lu, Jin Jian" uniqKey="Lu J" first="Jin-Jian" last="Lu">Jin-Jian Lu</name><affiliation wicri:level="1"><nlm:affiliation>State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao, China. Electronic address: jinjianlu@umac.mo.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao</wicri:regionArea><wicri:noRegion>Macao</wicri:noRegion></affiliation></author></analytic><series><title level="j">Redox biology</title><idno type="eISSN">2213-2317</idno><imprint><date when="2017" type="published">2017</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>A549 Cells</term><term>Antineoplastic Agents (pharmacology)</term><term>Autophagy</term><term>Benzophenanthridines (pharmacology)</term><term>Carcinoma, Non-Small-Cell Lung (metabolism)</term><term>Cell Line, Tumor</term><term>Cell Proliferation (drug effects)</term><term>Cell Survival (drug effects)</term><term>Dose-Response Relationship, Drug</term><term>Gene Expression Regulation, Neoplastic (drug effects)</term><term>Humans</term><term>Lung Neoplasms (metabolism)</term><term>Microtubule-Associated Proteins (metabolism)</term><term>Reactive Oxygen Species (metabolism)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Antinéoplasiques (pharmacologie)</term><term>Autophagie</term><term>Benzophénanthridines (pharmacologie)</term><term>Carcinome pulmonaire non à petites cellules (métabolisme)</term><term>Cellules A549</term><term>Espèces réactives de l'oxygène (métabolisme)</term><term>Humains</term><term>Lignée cellulaire tumorale</term><term>Prolifération cellulaire ()</term><term>Protéines associées aux microtubules (métabolisme)</term><term>Relation dose-effet des médicaments</term><term>Régulation de l'expression des gènes tumoraux ()</term><term>Survie cellulaire ()</term><term>Tumeurs du poumon (métabolisme)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Microtubule-Associated Proteins</term><term>Reactive Oxygen Species</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Antineoplastic Agents</term><term>Benzophenanthridines</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Cell Proliferation</term><term>Cell Survival</term><term>Gene Expression Regulation, Neoplastic</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>Carcinome pulmonaire non à petites cellules</term><term>Espèces réactives de l'oxygène</term><term>Protéines associées aux microtubules</term><term>Tumeurs du poumon</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Antinéoplasiques</term><term>Benzophénanthridines</term></keywords><keywords scheme="MESH" xml:lang="en"><term>A549 Cells</term><term>Autophagy</term><term>Cell Line, Tumor</term><term>Dose-Response Relationship, Drug</term><term>Humans</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Autophagie</term><term>Cellules A549</term><term>Humains</term><term>Lignée cellulaire tumorale</term><term>Prolifération cellulaire</term><term>Relation dose-effet des médicaments</term><term>Régulation de l'expression des gènes tumoraux</term><term>Survie cellulaire</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Chelerythrine (CHE), a natural benzo[c]phenanthridine alkaloid, shows anti-cancer effect through a number of mechanisms. Herein, the effect and mechanism of the CHE-induced autophagy, a type II programmed cell death, in non-small cell lung cancer (NSCLC) cells were studied for the first time. CHE induced cell viability decrease, colony formation inhibition, and apoptosis in a concentration-dependent manner in NSCLC A549 and NCI-H1299 cells. In addition, CHE triggered the expression of phosphatidylethanolamine-modified microtubule-associated protein light-chain 3 (LC3-II). The CHE-induced expression of LC3-II was further increased in the combination treatment with chloroquine (CQ), an autophagy inhibitor, and large amounts of red-puncta were observed in the CHE-treated A549 cells with stable expression of mRFP-EGFP-LC3, indicating that CHE induces autophagy flux. Silence of beclin 1 reversed the CHE-induced expression of LC3-II. Inhibition of autophagy remarkably reversed the CHE-induced cell viability decrease and apoptosis in NCI-H1299 cells but not in A549 cells. Furthermore, CHE triggered reactive oxygen species (ROS) generation in both cell lines. A decreased level of ROS through pretreatment with N-acetyl-L-cysteine reversed the CHE-induced cell viability decrease, apoptosis, and autophagy. Taken together, CHE induced distinctive autophagy in A549 (accompanied autophagy) and NCI-H1299 (pro-death autophagy) cells and a decreased level of ROS reversed the effect of CHE in NSCLC cells in terms of cell viability, apoptosis, and autophagy.</div></front></TEI><affiliations><list><country><li>République populaire de Chine</li></country><region><li>Guangdong</li></region><settlement><li>Jiangmen</li></settlement></list><tree><country name="République populaire de Chine"><noRegion><name sortKey="Tang, Zheng Hai" sort="Tang, Zheng Hai" uniqKey="Tang Z" first="Zheng-Hai" last="Tang">Zheng-Hai Tang</name></noRegion><name sortKey="Cao, Wen Xiang" sort="Cao, Wen Xiang" uniqKey="Cao W" first="Wen-Xiang" last="Cao">Wen-Xiang Cao</name><name sortKey="Chen, Xiuping" sort="Chen, Xiuping" uniqKey="Chen X" first="Xiuping" last="Chen">Xiuping Chen</name><name sortKey="Liu, Bo" sort="Liu, Bo" uniqKey="Liu B" first="Bo" last="Liu">Bo Liu</name><name sortKey="Lu, Jia Hong" sort="Lu, Jia Hong" uniqKey="Lu J" first="Jia-Hong" last="Lu">Jia-Hong Lu</name><name sortKey="Lu, Jin Jian" sort="Lu, Jin Jian" uniqKey="Lu J" first="Jin-Jian" last="Lu">Jin-Jian Lu</name><name sortKey="Wang, Zhao Yu" sort="Wang, Zhao Yu" uniqKey="Wang Z" first="Zhao-Yu" last="Wang">Zhao-Yu Wang</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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