Induction of C/EBP homologous protein-mediated apoptosis and autophagy by licochalcone A in non-small cell lung cancer cells.
Identifieur interne : 000340 ( Ncbi/Checkpoint ); précédent : 000339; suivant : 000341Induction of C/EBP homologous protein-mediated apoptosis and autophagy by licochalcone A in non-small cell lung cancer cells.
Auteurs : Zheng-Hai Tang [République populaire de Chine] ; Xin Chen [République populaire de Chine] ; Zhao-Yu Wang [République populaire de Chine] ; Ke Chai [République populaire de Chine] ; Ya-Fang Wang [République populaire de Chine] ; Xiao-Huang Xu [République populaire de Chine] ; Xiao-Wen Wang [République populaire de Chine] ; Jia-Hong Lu [République populaire de Chine] ; Yi-Tao Wang [République populaire de Chine] ; Xiu-Ping Chen [République populaire de Chine] ; Jin-Jian Lu [République populaire de Chine]Source :
- Scientific reports [ 2045-2322 ] ; 2016.
Descripteurs français
- KwdFr :
- Antinéoplasiques d'origine végétale (pharmacologie), Apoptose (), Autophagie (), Carcinome pulmonaire non à petites cellules (anatomopathologie), Carcinome pulmonaire non à petites cellules (métabolisme), Carcinome pulmonaire non à petites cellules (traitement médicamenteux), Cellules A549, Chalcones (pharmacologie), Facteur de transcription CHOP (antagonistes et inhibiteurs), Facteur de transcription CHOP (génétique), Facteur de transcription CHOP (métabolisme), Glycyrrhiza uralensis (), Humains, L-Lactate dehydrogenase (métabolisme), Lignée cellulaire tumorale, Médicaments issus de plantes chinoises (pharmacologie), Protéines associées aux microtubules (métabolisme), Survie cellulaire (), Techniques de knock-down de gènes, Tumeurs du poumon (anatomopathologie), Tumeurs du poumon (métabolisme), Tumeurs du poumon (traitement médicamenteux).
- MESH :
- anatomopathologie : Carcinome pulmonaire non à petites cellules, Tumeurs du poumon.
- antagonistes et inhibiteurs : Facteur de transcription CHOP.
- génétique : Facteur de transcription CHOP.
- métabolisme : Carcinome pulmonaire non à petites cellules, Facteur de transcription CHOP, L-Lactate dehydrogenase, Protéines associées aux microtubules, Tumeurs du poumon.
- pharmacologie : Antinéoplasiques d'origine végétale, Chalcones, Médicaments issus de plantes chinoises.
- traitement médicamenteux : Carcinome pulmonaire non à petites cellules, Tumeurs du poumon.
- Apoptose, Autophagie, Cellules A549, Glycyrrhiza uralensis, Humains, Lignée cellulaire tumorale, Survie cellulaire, Techniques de knock-down de gènes.
English descriptors
- KwdEn :
- A549 Cells, Antineoplastic Agents, Phytogenic (pharmacology), Apoptosis (drug effects), Autophagy (drug effects), Carcinoma, Non-Small-Cell Lung (drug therapy), Carcinoma, Non-Small-Cell Lung (metabolism), Carcinoma, Non-Small-Cell Lung (pathology), Cell Line, Tumor, Cell Survival (drug effects), Chalcones (pharmacology), Drugs, Chinese Herbal (pharmacology), Gene Knockdown Techniques, Glycyrrhiza uralensis (chemistry), Humans, L-Lactate Dehydrogenase (metabolism), Lung Neoplasms (drug therapy), Lung Neoplasms (metabolism), Lung Neoplasms (pathology), Microtubule-Associated Proteins (metabolism), Transcription Factor CHOP (antagonists & inhibitors), Transcription Factor CHOP (genetics), Transcription Factor CHOP (metabolism).
- MESH :
- chemical , antagonists & inhibitors : Transcription Factor CHOP.
- chemical , genetics : Transcription Factor CHOP.
- chemical , metabolism : L-Lactate Dehydrogenase, Microtubule-Associated Proteins, Transcription Factor CHOP.
- chemical , pharmacology : Antineoplastic Agents, Phytogenic, Chalcones, Drugs, Chinese Herbal.
- chemistry : Glycyrrhiza uralensis.
- drug effects : Apoptosis, Autophagy, Cell Survival.
- drug therapy : Carcinoma, Non-Small-Cell Lung, Lung Neoplasms.
- metabolism : Carcinoma, Non-Small-Cell Lung, Lung Neoplasms.
- pathology : Carcinoma, Non-Small-Cell Lung, Lung Neoplasms.
- A549 Cells, Cell Line, Tumor, Gene Knockdown Techniques, Humans.
Abstract
Licochalcone A (LCA), a flavonoid isolated from the famous Chinese medicinal herb Glycyrrhiza uralensis Fisch, presents obvious anti-cancer effects. In this study, the anti-cancer effects and potential mechanisms of LCA in non-small cell lung cancer (NSCLC) cells were studied. LCA decreased cell viability, increased lactate dehydrogenase release, and induced apoptosis in a concentration-dependent manner in NSCLC cells while not in human embryonic lung fibroblast cells. The expression of phosphatidylethanolamine-modified microtubule-associated protein light-chain 3 (LC3-II) and formation of GFP-LC3 punta, two autophagic markers, were increased after treatment with LCA. LCA-induced LC3-II expression was increased when combined with chloroquine (CQ), while knock-down of autophagy related protein (ATG) 7 or ATG5 reversed LCA-induced LC3-II expression and GFP-LC3 punta formation, suggesting that LCA induced autophagy in NSCLC cells. Inhibition of autophagy could not reverse the LCA-induced cell viability decrease and apoptosis. In addition, LCA increased the expression of endoplasmic reticulum stress related proteins, such as binding immunoglobulin protein and C/EBP homologous protein (CHOP). Knock-down of CHOP reversed LCA-induced cell viability decrease, apoptosis, and autophagy. Taken together, LCA-induced autophagic effect is an accompanied phenomenon in NSCLC cells, and CHOP is critical for LCA-induced cell viability decrease, apoptosis, and autophagy.
DOI: 10.1038/srep26241
PubMed: 27184816
Affiliations:
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pubmed:27184816Le document en format XML
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<term>Antineoplastic Agents, Phytogenic (pharmacology)</term>
<term>Apoptosis (drug effects)</term>
<term>Autophagy (drug effects)</term>
<term>Carcinoma, Non-Small-Cell Lung (drug therapy)</term>
<term>Carcinoma, Non-Small-Cell Lung (metabolism)</term>
<term>Carcinoma, Non-Small-Cell Lung (pathology)</term>
<term>Cell Line, Tumor</term>
<term>Cell Survival (drug effects)</term>
<term>Chalcones (pharmacology)</term>
<term>Drugs, Chinese Herbal (pharmacology)</term>
<term>Gene Knockdown Techniques</term>
<term>Glycyrrhiza uralensis (chemistry)</term>
<term>Humans</term>
<term>L-Lactate Dehydrogenase (metabolism)</term>
<term>Lung Neoplasms (drug therapy)</term>
<term>Lung Neoplasms (metabolism)</term>
<term>Lung Neoplasms (pathology)</term>
<term>Microtubule-Associated Proteins (metabolism)</term>
<term>Transcription Factor CHOP (antagonists & inhibitors)</term>
<term>Transcription Factor CHOP (genetics)</term>
<term>Transcription Factor CHOP (metabolism)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Antinéoplasiques d'origine végétale (pharmacologie)</term>
<term>Apoptose ()</term>
<term>Autophagie ()</term>
<term>Carcinome pulmonaire non à petites cellules (anatomopathologie)</term>
<term>Carcinome pulmonaire non à petites cellules (métabolisme)</term>
<term>Carcinome pulmonaire non à petites cellules (traitement médicamenteux)</term>
<term>Cellules A549</term>
<term>Chalcones (pharmacologie)</term>
<term>Facteur de transcription CHOP (antagonistes et inhibiteurs)</term>
<term>Facteur de transcription CHOP (génétique)</term>
<term>Facteur de transcription CHOP (métabolisme)</term>
<term>Glycyrrhiza uralensis ()</term>
<term>Humains</term>
<term>L-Lactate dehydrogenase (métabolisme)</term>
<term>Lignée cellulaire tumorale</term>
<term>Médicaments issus de plantes chinoises (pharmacologie)</term>
<term>Protéines associées aux microtubules (métabolisme)</term>
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<term>Tumeurs du poumon (métabolisme)</term>
<term>Tumeurs du poumon (traitement médicamenteux)</term>
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<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Transcription Factor CHOP</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>L-Lactate Dehydrogenase</term>
<term>Microtubule-Associated Proteins</term>
<term>Transcription Factor CHOP</term>
</keywords>
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<term>Drugs, Chinese Herbal</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="antagonistes et inhibiteurs" xml:lang="fr"><term>Facteur de transcription CHOP</term>
</keywords>
<keywords scheme="MESH" qualifier="chemistry" xml:lang="en"><term>Glycyrrhiza uralensis</term>
</keywords>
<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Apoptosis</term>
<term>Autophagy</term>
<term>Cell Survival</term>
</keywords>
<keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Carcinoma, Non-Small-Cell Lung</term>
<term>Lung Neoplasms</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Facteur de transcription CHOP</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>Facteur de transcription CHOP</term>
<term>L-Lactate dehydrogenase</term>
<term>Protéines associées aux microtubules</term>
<term>Tumeurs du poumon</term>
</keywords>
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<term>Lung Neoplasms</term>
</keywords>
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<term>Chalcones</term>
<term>Médicaments issus de plantes chinoises</term>
</keywords>
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<term>Tumeurs du poumon</term>
</keywords>
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<term>Gene Knockdown Techniques</term>
<term>Humans</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Apoptose</term>
<term>Autophagie</term>
<term>Cellules A549</term>
<term>Glycyrrhiza uralensis</term>
<term>Humains</term>
<term>Lignée cellulaire tumorale</term>
<term>Survie cellulaire</term>
<term>Techniques de knock-down de gènes</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en">Licochalcone A (LCA), a flavonoid isolated from the famous Chinese medicinal herb Glycyrrhiza uralensis Fisch, presents obvious anti-cancer effects. In this study, the anti-cancer effects and potential mechanisms of LCA in non-small cell lung cancer (NSCLC) cells were studied. LCA decreased cell viability, increased lactate dehydrogenase release, and induced apoptosis in a concentration-dependent manner in NSCLC cells while not in human embryonic lung fibroblast cells. The expression of phosphatidylethanolamine-modified microtubule-associated protein light-chain 3 (LC3-II) and formation of GFP-LC3 punta, two autophagic markers, were increased after treatment with LCA. LCA-induced LC3-II expression was increased when combined with chloroquine (CQ), while knock-down of autophagy related protein (ATG) 7 or ATG5 reversed LCA-induced LC3-II expression and GFP-LC3 punta formation, suggesting that LCA induced autophagy in NSCLC cells. Inhibition of autophagy could not reverse the LCA-induced cell viability decrease and apoptosis. In addition, LCA increased the expression of endoplasmic reticulum stress related proteins, such as binding immunoglobulin protein and C/EBP homologous protein (CHOP). Knock-down of CHOP reversed LCA-induced cell viability decrease, apoptosis, and autophagy. Taken together, LCA-induced autophagic effect is an accompanied phenomenon in NSCLC cells, and CHOP is critical for LCA-induced cell viability decrease, apoptosis, and autophagy.</div>
</front>
</TEI>
<affiliations><list><country><li>République populaire de Chine</li>
</country>
<settlement><li>Pékin</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="Chai, Ke" sort="Chai, Ke" uniqKey="Chai K" first="Ke" last="Chai">Ke Chai</name>
<name sortKey="Chen, Xin" sort="Chen, Xin" uniqKey="Chen X" first="Xin" last="Chen">Xin Chen</name>
<name sortKey="Chen, Xiu Ping" sort="Chen, Xiu Ping" uniqKey="Chen X" first="Xiu-Ping" last="Chen">Xiu-Ping Chen</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, Xiao Wen" sort="Wang, Xiao Wen" uniqKey="Wang X" first="Xiao-Wen" last="Wang">Xiao-Wen Wang</name>
<name sortKey="Wang, Ya Fang" sort="Wang, Ya Fang" uniqKey="Wang Y" first="Ya-Fang" last="Wang">Ya-Fang Wang</name>
<name sortKey="Wang, Yi Tao" sort="Wang, Yi Tao" uniqKey="Wang Y" first="Yi-Tao" last="Wang">Yi-Tao Wang</name>
<name sortKey="Wang, Zhao Yu" sort="Wang, Zhao Yu" uniqKey="Wang Z" first="Zhao-Yu" last="Wang">Zhao-Yu Wang</name>
<name sortKey="Xu, Xiao Huang" sort="Xu, Xiao Huang" uniqKey="Xu X" first="Xiao-Huang" last="Xu">Xiao-Huang Xu</name>
</country>
</tree>
</affiliations>
</record>
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