[Inhibition of autophagy initiation stage enhances camptothecin-induced apoptosis in NCI-H1975 cells].
Identifieur interne : 000135 ( PubMed/Checkpoint ); précédent : 000134; suivant : 000136[Inhibition of autophagy initiation stage enhances camptothecin-induced apoptosis in NCI-H1975 cells].
Auteurs : Yaping Zhang [République populaire de Chine] ; Li Cao [République populaire de Chine] ; Qiang Su [République populaire de Chine] ; Kai Cheng [République populaire de Chine] ; Xiaoyan Zhang [Oman]Source :
- Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology [ 1007-8738 ] ; 2017.
Descripteurs français
- KwdFr :
- Adénine (analogues et dérivés), Adénine (pharmacologie), Apoptose (), Autophagie (), Camptothécine (pharmacologie), Carcinome pulmonaire non à petites cellules (anatomopathologie), Carcinome pulmonaire non à petites cellules (traitement médicamenteux), Chloroquine (pharmacologie), Facteur de croissance transformant bêta-1 (analyse), Humains, Lignée cellulaire tumorale, Prolifération cellulaire (), Tumeurs du poumon (anatomopathologie), Tumeurs du poumon (traitement médicamenteux).
- MESH :
- analogues et dérivés : Adénine.
- analyse : Facteur de croissance transformant bêta-1.
- anatomopathologie : Carcinome pulmonaire non à petites cellules, Tumeurs du poumon.
- pharmacologie : Adénine, Camptothécine, Chloroquine.
- traitement médicamenteux : Carcinome pulmonaire non à petites cellules, Tumeurs du poumon.
- Apoptose, Autophagie, Humains, Lignée cellulaire tumorale, Prolifération cellulaire.
English descriptors
- KwdEn :
- Adenine (analogs & derivatives), Adenine (pharmacology), Apoptosis (drug effects), Autophagy (drug effects), Camptothecin (pharmacology), Carcinoma, Non-Small-Cell Lung (drug therapy), Carcinoma, Non-Small-Cell Lung (pathology), Cell Line, Tumor, Cell Proliferation (drug effects), Chloroquine (pharmacology), Humans, Lung Neoplasms (drug therapy), Lung Neoplasms (pathology), Transforming Growth Factor beta1 (analysis).
- MESH :
- chemical , analogs & derivatives : Adenine.
- chemical , analysis : Transforming Growth Factor beta1.
- chemical , pharmacology : Adenine, Camptothecin, Chloroquine.
- drug effects : Apoptosis, Autophagy, Cell Proliferation.
- drug therapy : Carcinoma, Non-Small-Cell Lung, Lung Neoplasms.
- pathology : Carcinoma, Non-Small-Cell Lung, Lung Neoplasms.
- Cell Line, Tumor, Humans.
Abstract
Objective To explore the effect of autophagic inhibitors chloroquine (CQ) and 3-methyl adenine (3-MA) on apoptosis of non-small cell lung adenocarcinoma NCI-H1975 cells induced by camptothecin (CPT). Methods After NCI-H1975 cells were treated with CPT, cell proliferation was detected by CCK-8 assay, morphological changes of cells were observed by PI staining, and the apoptosis of NCI-H1975 cells was determined by flow cytometry. The levels of autophagy-and apoptosis-related proteins LC3I, LC3II, P62, caspase-3 and poly ADP-ribose polymerase (PARP) and transforming growth factor beta 1 (TGF-beta 1) were detected by Western blot analysis. Results After CPT treatment, the ratio of LC3II to LC3I was raised. The apoptotic protease caspase-3 and substrate PARP were obviously degraded, which could be enhanced by 3-MA but inhibited by CQ. It was also found that the intracellular TGF-beta 1 was reduced after CPT treatment. Conclusion Inhibition of autophagy initiation stage in NCI-H1975 cells can increase the sensitivity of cell apoptosis induced by CPT.
PubMed: 29382424
Affiliations:
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pubmed:29382424Le document en format XML
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<term>Carcinome pulmonaire non à petites cellules (anatomopathologie)</term>
<term>Carcinome pulmonaire non à petites cellules (traitement médicamenteux)</term>
<term>Chloroquine (pharmacologie)</term>
<term>Facteur de croissance transformant bêta-1 (analyse)</term>
<term>Humains</term>
<term>Lignée cellulaire tumorale</term>
<term>Prolifération cellulaire ()</term>
<term>Tumeurs du poumon (anatomopathologie)</term>
<term>Tumeurs du poumon (traitement médicamenteux)</term>
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<term>Chloroquine</term>
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<front><div type="abstract" xml:lang="en">Objective To explore the effect of autophagic inhibitors chloroquine (CQ) and 3-methyl adenine (3-MA) on apoptosis of non-small cell lung adenocarcinoma NCI-H1975 cells induced by camptothecin (CPT). Methods After NCI-H1975 cells were treated with CPT, cell proliferation was detected by CCK-8 assay, morphological changes of cells were observed by PI staining, and the apoptosis of NCI-H1975 cells was determined by flow cytometry. The levels of autophagy-and apoptosis-related proteins LC3I, LC3II, P62, caspase-3 and poly ADP-ribose polymerase (PARP) and transforming growth factor beta 1 (TGF-beta 1) were detected by Western blot analysis. Results After CPT treatment, the ratio of LC3II to LC3I was raised. The apoptotic protease caspase-3 and substrate PARP were obviously degraded, which could be enhanced by 3-MA but inhibited by CQ. It was also found that the intracellular TGF-beta 1 was reduced after CPT treatment. Conclusion Inhibition of autophagy initiation stage in NCI-H1975 cells can increase the sensitivity of cell apoptosis induced by CPT.</div>
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<Abstract><AbstractText>Objective To explore the effect of autophagic inhibitors chloroquine (CQ) and 3-methyl adenine (3-MA) on apoptosis of non-small cell lung adenocarcinoma NCI-H1975 cells induced by camptothecin (CPT). Methods After NCI-H1975 cells were treated with CPT, cell proliferation was detected by CCK-8 assay, morphological changes of cells were observed by PI staining, and the apoptosis of NCI-H1975 cells was determined by flow cytometry. The levels of autophagy-and apoptosis-related proteins LC3I, LC3II, P62, caspase-3 and poly ADP-ribose polymerase (PARP) and transforming growth factor beta 1 (TGF-beta 1) were detected by Western blot analysis. Results After CPT treatment, the ratio of LC3II to LC3I was raised. The apoptotic protease caspase-3 and substrate PARP were obviously degraded, which could be enhanced by 3-MA but inhibited by CQ. It was also found that the intracellular TGF-beta 1 was reduced after CPT treatment. Conclusion Inhibition of autophagy initiation stage in NCI-H1975 cells can increase the sensitivity of cell apoptosis induced by CPT.</AbstractText>
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