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[Inhibition of autophagy initiation stage enhances camptothecin-induced apoptosis in NCI-H1975 cells].

Identifieur interne : 000C84 ( Main/Exploration ); précédent : 000C83; suivant : 000C85

[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]

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RBID : pubmed:29382424

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English descriptors

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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<term>Adenine (pharmacology)</term>
<term>Apoptosis (drug effects)</term>
<term>Autophagy (drug effects)</term>
<term>Camptothecin (pharmacology)</term>
<term>Carcinoma, Non-Small-Cell Lung (drug therapy)</term>
<term>Carcinoma, Non-Small-Cell Lung (pathology)</term>
<term>Cell Line, Tumor</term>
<term>Cell Proliferation (drug effects)</term>
<term>Chloroquine (pharmacology)</term>
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<term>Lung Neoplasms (drug therapy)</term>
<term>Lung Neoplasms (pathology)</term>
<term>Transforming Growth Factor beta1 (analysis)</term>
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<term>Adénine (analogues et dérivés)</term>
<term>Adénine (pharmacologie)</term>
<term>Apoptose ()</term>
<term>Autophagie ()</term>
<term>Camptothécine (pharmacologie)</term>
<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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<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en">
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<term>Camptothecin</term>
<term>Chloroquine</term>
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<term>Apoptosis</term>
<term>Autophagy</term>
<term>Cell Proliferation</term>
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<term>Lung Neoplasms</term>
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<term>Adénine</term>
<term>Camptothécine</term>
<term>Chloroquine</term>
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<term>Carcinome pulmonaire non à petites cellules</term>
<term>Tumeurs du poumon</term>
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<term>Humans</term>
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<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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