Inhibition of autophagy enhances effects of PF-04691502 on apoptosis and DNA damage of lung cancer cells.
Identifieur interne : 000D68 ( Main/Exploration ); précédent : 000D67; suivant : 000D69Inhibition of autophagy enhances effects of PF-04691502 on apoptosis and DNA damage of lung cancer cells.
Auteurs : Hong-Rong Fei [République populaire de Chine] ; Hua- Tian [République populaire de Chine] ; Xiao-Lei Zhou [République populaire de Chine] ; Ming-Feng Yang [République populaire de Chine] ; Bao-Liang Sun [République populaire de Chine] ; Xiao-Yi Yang [République populaire de Chine] ; Peng- Jiao [République populaire de Chine] ; Feng-Ze Wang [République populaire de Chine]Source :
- The international journal of biochemistry & cell biology [ 1878-5875 ] ; 2016.
Descripteurs français
- KwdFr :
- Altération de l'ADN, Antinéoplasiques (pharmacologie), Apoptose (), Autophagie (), Carcinome pulmonaire non à petites cellules (anatomopathologie), Histone (métabolisme), Humains, Lignée cellulaire tumorale, Phosphorylation (), Points de contrôle de la phase G1 du cycle cellulaire (), Protéines proto-oncogènes c-akt (métabolisme), Pyridones (pharmacologie), Pyrimidines (pharmacologie), Relation dose-effet des médicaments, Survie cellulaire (), Tumeurs du poumon (anatomopathologie).
- MESH :
- anatomopathologie : Carcinome pulmonaire non à petites cellules, Tumeurs du poumon.
- métabolisme : Histone, Protéines proto-oncogènes c-akt.
- pharmacologie : Antinéoplasiques, Pyridones, Pyrimidines.
- Altération de l'ADN, Apoptose, Autophagie, Humains, Lignée cellulaire tumorale, Phosphorylation, Points de contrôle de la phase G1 du cycle cellulaire, Relation dose-effet des médicaments, Survie cellulaire.
English descriptors
- KwdEn :
- Antineoplastic Agents (pharmacology), Apoptosis (drug effects), Autophagy (drug effects), Carcinoma, Non-Small-Cell Lung (pathology), Cell Line, Tumor, Cell Survival (drug effects), DNA Damage, Dose-Response Relationship, Drug, G1 Phase Cell Cycle Checkpoints (drug effects), Histones (metabolism), Humans, Lung Neoplasms (pathology), Phosphorylation (drug effects), Proto-Oncogene Proteins c-akt (metabolism), Pyridones (pharmacology), Pyrimidines (pharmacology).
- MESH :
- chemical , metabolism : Histones, Proto-Oncogene Proteins c-akt.
- chemical , pharmacology : Antineoplastic Agents, Pyridones, Pyrimidines.
- drug effects : Apoptosis, Autophagy, Cell Survival, G1 Phase Cell Cycle Checkpoints, Phosphorylation.
- pathology : Carcinoma, Non-Small-Cell Lung, Lung Neoplasms.
- Cell Line, Tumor, DNA Damage, Dose-Response Relationship, Drug, Humans.
Abstract
Autophagy modulation has been considered as a potential therapeutic strategy for lung diseases. The PI3K-Akt-mTOR pathway may be one of the main targets for regulation of autophagy. We previously reported that a PI3K/mTOR dual inhibitor PF-04691502 suppressed hepatoma cells growth in vitro. However, it is still unclear whether PF-04691502 induces autophagy and its roles in DNA damage and cell death in human lung cancer cells. In this study, we investigate the effects of PF-04691502 on the autophagy and its correlation with cell apoptosis and DNA damage in non-small-cell lung cancer (NSCLC) cell lines. PF-04691502 efficiently inhibited the phosphorylation of Akt and showed dose-dependent cytotoxicity in A549 and H1299 cells. PF-04691502 also triggered apoptosis and the cleavage of caspase-3 and PARP. Phosphorylated histone H2AX (γ-H2AX), a hallmark of DNA damage response, was dramatically induced by PF-04691502 treatment. By exposure to PF-04691502, A549 cells acquired a senescent-like phenotype with an increase in the level of β-galactosidase. Furthermore, PF-04691502 enhanced the expression of LC3-II in a concentration-dependent manner. More interestingly, effects of PF-04691502 on toxicity and DNA damage were remarkably increased by co-treatment with an autophagy inhibitor, chloroquine (CQ), in human lung cancer cells. These data suggest that a strategy of blocking autophagy to enhance the activity of PI3K/mTOR inhibitors warrants further attention in treatment of NSCLC cells.
DOI: 10.1016/j.biocel.2016.06.023
PubMed: 27378731
Affiliations:
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Electronic address: jiaopeng196@163.com.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Key Laboratory of Atherosclerosis in Universities of Shandong, Taishan Medical University, Taian, 271000</wicri:regionArea><wicri:noRegion>271000</wicri:noRegion></affiliation></author><author><name sortKey="Wang, Feng Ze" sort="Wang, Feng Ze" uniqKey="Wang F" first="Feng-Ze" last="Wang">Feng-Ze Wang</name><affiliation wicri:level="1"><nlm:affiliation>Key Laboratory of Brain Microcirculation in Universities of Shandong, Taishan Medical University, Taian, 271000, PR China; School of Life Sciences, Taishan Medical University, Taian, 271016, PR China. 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Electronic address: xyyang@tsmc.edu.cn.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Key Laboratory of Brain Microcirculation in Universities of Shandong, Taishan Medical University, Taian, 271000</wicri:regionArea><wicri:noRegion>271000</wicri:noRegion></affiliation></author><author><name sortKey="Jiao, Peng" sort="Jiao, Peng" uniqKey="Jiao P" first="Peng-" last="Jiao">Peng- Jiao</name><affiliation wicri:level="1"><nlm:affiliation>Key Laboratory of Atherosclerosis in Universities of Shandong, Taishan Medical University, Taian, 271000, PR China. Electronic address: jiaopeng196@163.com.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Key Laboratory of Atherosclerosis in Universities of Shandong, Taishan Medical University, Taian, 271000</wicri:regionArea><wicri:noRegion>271000</wicri:noRegion></affiliation></author><author><name sortKey="Wang, Feng Ze" sort="Wang, Feng Ze" uniqKey="Wang F" first="Feng-Ze" last="Wang">Feng-Ze Wang</name><affiliation wicri:level="1"><nlm:affiliation>Key Laboratory of Brain Microcirculation in Universities of Shandong, Taishan Medical University, Taian, 271000, PR China; School of Life Sciences, Taishan Medical University, Taian, 271016, PR China. Electronic address: fengzewang@gmail.com.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Key Laboratory of Brain Microcirculation in Universities of Shandong, Taishan Medical University, Taian, 271000, PR China; School of Life Sciences, Taishan Medical University, Taian, 271016</wicri:regionArea><wicri:noRegion>271016</wicri:noRegion></affiliation></author></analytic><series><title level="j">The international journal of biochemistry & cell biology</title><idno type="eISSN">1878-5875</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>Carcinoma, Non-Small-Cell Lung (pathology)</term><term>Cell Line, Tumor</term><term>Cell Survival (drug effects)</term><term>DNA Damage</term><term>Dose-Response Relationship, Drug</term><term>G1 Phase Cell Cycle Checkpoints (drug effects)</term><term>Histones (metabolism)</term><term>Humans</term><term>Lung Neoplasms (pathology)</term><term>Phosphorylation (drug effects)</term><term>Proto-Oncogene Proteins c-akt (metabolism)</term><term>Pyridones (pharmacology)</term><term>Pyrimidines (pharmacology)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Altération de l'ADN</term><term>Antinéoplasiques (pharmacologie)</term><term>Apoptose ()</term><term>Autophagie ()</term><term>Carcinome pulmonaire non à petites cellules (anatomopathologie)</term><term>Histone (métabolisme)</term><term>Humains</term><term>Lignée cellulaire tumorale</term><term>Phosphorylation ()</term><term>Points de contrôle de la phase G1 du cycle cellulaire ()</term><term>Protéines proto-oncogènes c-akt (métabolisme)</term><term>Pyridones (pharmacologie)</term><term>Pyrimidines (pharmacologie)</term><term>Relation dose-effet des médicaments</term><term>Survie cellulaire ()</term><term>Tumeurs du poumon (anatomopathologie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Histones</term><term>Proto-Oncogene Proteins c-akt</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Antineoplastic Agents</term><term>Pyridones</term><term>Pyrimidines</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Carcinome pulmonaire non à petites cellules</term><term>Tumeurs du poumon</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Apoptosis</term><term>Autophagy</term><term>Cell Survival</term><term>G1 Phase Cell Cycle Checkpoints</term><term>Phosphorylation</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Histone</term><term>Protéines proto-oncogènes c-akt</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Carcinoma, Non-Small-Cell Lung</term><term>Lung Neoplasms</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Antinéoplasiques</term><term>Pyridones</term><term>Pyrimidines</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Cell Line, Tumor</term><term>DNA Damage</term><term>Dose-Response Relationship, Drug</term><term>Humans</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Altération de l'ADN</term><term>Apoptose</term><term>Autophagie</term><term>Humains</term><term>Lignée cellulaire tumorale</term><term>Phosphorylation</term><term>Points de contrôle de la phase G1 du cycle cellulaire</term><term>Relation dose-effet des médicaments</term><term>Survie cellulaire</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Autophagy modulation has been considered as a potential therapeutic strategy for lung diseases. The PI3K-Akt-mTOR pathway may be one of the main targets for regulation of autophagy. We previously reported that a PI3K/mTOR dual inhibitor PF-04691502 suppressed hepatoma cells growth in vitro. However, it is still unclear whether PF-04691502 induces autophagy and its roles in DNA damage and cell death in human lung cancer cells. In this study, we investigate the effects of PF-04691502 on the autophagy and its correlation with cell apoptosis and DNA damage in non-small-cell lung cancer (NSCLC) cell lines. PF-04691502 efficiently inhibited the phosphorylation of Akt and showed dose-dependent cytotoxicity in A549 and H1299 cells. PF-04691502 also triggered apoptosis and the cleavage of caspase-3 and PARP. Phosphorylated histone H2AX (γ-H2AX), a hallmark of DNA damage response, was dramatically induced by PF-04691502 treatment. By exposure to PF-04691502, A549 cells acquired a senescent-like phenotype with an increase in the level of β-galactosidase. Furthermore, PF-04691502 enhanced the expression of LC3-II in a concentration-dependent manner. More interestingly, effects of PF-04691502 on toxicity and DNA damage were remarkably increased by co-treatment with an autophagy inhibitor, chloroquine (CQ), in human lung cancer cells. These data suggest that a strategy of blocking autophagy to enhance the activity of PI3K/mTOR inhibitors warrants further attention in treatment of NSCLC cells.</div></front></TEI><affiliations><list><country><li>République populaire de Chine</li></country></list><tree><country name="République populaire de Chine"><noRegion><name sortKey="Fei, Hong Rong" sort="Fei, Hong Rong" uniqKey="Fei H" first="Hong-Rong" last="Fei">Hong-Rong Fei</name></noRegion><name sortKey="Jiao, Peng" sort="Jiao, Peng" uniqKey="Jiao P" first="Peng-" last="Jiao">Peng- Jiao</name><name sortKey="Sun, Bao Liang" sort="Sun, Bao Liang" uniqKey="Sun B" first="Bao-Liang" last="Sun">Bao-Liang Sun</name><name sortKey="Tian, Hua" sort="Tian, Hua" uniqKey="Tian H" first="Hua-" last="Tian">Hua- Tian</name><name sortKey="Wang, Feng Ze" sort="Wang, Feng Ze" uniqKey="Wang F" first="Feng-Ze" last="Wang">Feng-Ze Wang</name><name sortKey="Yang, Ming Feng" sort="Yang, Ming Feng" uniqKey="Yang M" first="Ming-Feng" last="Yang">Ming-Feng Yang</name><name sortKey="Yang, Xiao Yi" sort="Yang, Xiao Yi" uniqKey="Yang X" first="Xiao-Yi" last="Yang">Xiao-Yi Yang</name><name sortKey="Zhou, Xiao Lei" sort="Zhou, Xiao Lei" uniqKey="Zhou X" first="Xiao-Lei" last="Zhou">Xiao-Lei Zhou</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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