Inhibition of autophagy by autophagic inhibitors enhances apoptosis induced by bortezomib in non-small cell lung cancer cells.
Identifieur interne : 001018 ( Main/Exploration ); précédent : 001017; suivant : 001019Inhibition of autophagy by autophagic inhibitors enhances apoptosis induced by bortezomib in non-small cell lung cancer cells.
Auteurs : Guodong Wu [Oman] ; Haifeng Li ; Zhiyong Ji ; Xiaoming Jiang ; Yu Lei ; Mingli SunSource :
- Biotechnology letters [ 1573-6776 ] ; 2014.
Descripteurs français
- KwdFr :
- Acides boroniques (métabolisme), Antinéoplasiques (métabolisme), Apoptose, Autophagie (), Bortézomib, Carcinome pulmonaire non à petites cellules, Caspase-3 (analyse), Cellules épithéliales (), Cytochromes c (analyse), Humains, Lignée cellulaire tumorale, Prolifération cellulaire (), Pyrazines (métabolisme).
- MESH :
English descriptors
- KwdEn :
- Antineoplastic Agents (metabolism), Apoptosis, Autophagy (drug effects), Boronic Acids (metabolism), Bortezomib, Carcinoma, Non-Small-Cell Lung, Caspase 3 (analysis), Cell Line, Tumor, Cell Proliferation (drug effects), Cytochromes c (analysis), Epithelial Cells (drug effects), Humans, Pyrazines (metabolism).
- MESH :
- chemical , analysis : Caspase 3, Cytochromes c.
- chemical , metabolism : Antineoplastic Agents, Boronic Acids, Pyrazines.
- drug effects : Autophagy, Cell Proliferation, Epithelial Cells.
- Apoptosis, Bortezomib, Carcinoma, Non-Small-Cell Lung, Cell Line, Tumor, Humans.
Abstract
Bortezomib is a novel proteasome inhibitor that has promising antitumor activity against various cancer cells. We have assessed its antitumor activity in non-small cell lung cancer (NSCLC) A549 and H157 cells in vitro where it inhibited cell growth and induced apoptosis, which was associated with cytochrome c release and caspase-3 activation. Bortezomib upregulated autophagic-related proteins, the Atg12-Atg5 complex and LC3-II, which indicated autophagy had occurred. The combination of bortezomib with autophagic inhibitor 3-methyladenine or chloroquine significantly enhanced suppression of cell growth and apoptosis induced by bortezomib in A549 and H157 cells. Our study indicated that inhibition of both proteasome and autophagy has great potential for NSCLC treatment.
DOI: 10.1007/s10529-014-1470-0
PubMed: 24563301
Affiliations:
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Le document en format XML
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<term>Bortezomib</term>
<term>Carcinoma, Non-Small-Cell Lung</term>
<term>Caspase 3 (analysis)</term>
<term>Cell Line, Tumor</term>
<term>Cell Proliferation (drug effects)</term>
<term>Cytochromes c (analysis)</term>
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<term>Bortézomib</term>
<term>Carcinome pulmonaire non à petites cellules</term>
<term>Caspase-3 (analyse)</term>
<term>Cellules épithéliales ()</term>
<term>Cytochromes c (analyse)</term>
<term>Humains</term>
<term>Lignée cellulaire tumorale</term>
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<term>Pyrazines (métabolisme)</term>
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<term>Pyrazines</term>
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<term>Antinéoplasiques</term>
<term>Pyrazines</term>
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<term>Bortezomib</term>
<term>Carcinoma, Non-Small-Cell Lung</term>
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<front><div type="abstract" xml:lang="en">Bortezomib is a novel proteasome inhibitor that has promising antitumor activity against various cancer cells. We have assessed its antitumor activity in non-small cell lung cancer (NSCLC) A549 and H157 cells in vitro where it inhibited cell growth and induced apoptosis, which was associated with cytochrome c release and caspase-3 activation. Bortezomib upregulated autophagic-related proteins, the Atg12-Atg5 complex and LC3-II, which indicated autophagy had occurred. The combination of bortezomib with autophagic inhibitor 3-methyladenine or chloroquine significantly enhanced suppression of cell growth and apoptosis induced by bortezomib in A549 and H157 cells. Our study indicated that inhibition of both proteasome and autophagy has great potential for NSCLC treatment. </div>
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<name sortKey="Lei, Yu" sort="Lei, Yu" uniqKey="Lei Y" first="Yu" last="Lei">Yu Lei</name>
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