ChloroquineV1, Ncbi, Merge, bibRecord, 000340

Induction of C/EBP homologous protein-mediated apoptosis and autophagy by licochalcone A in non-small cell lung cancer cells.

Identifieur interne : 000340 ( Ncbi/Merge ); précédent : 000339; suivant : 000341

Induction of C/EBP homologous protein-mediated apoptosis and autophagy by licochalcone A in non-small cell lung cancer cells.

Source :

Scientific reports [ 2045-2322 ] ; 2016.

RBID : pubmed:27184816

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

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Le document en format XML

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<term>Protéines associées aux microtubules</term>
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<term>Chalcones</term>
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<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>
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<DateCompleted><Year>2018</Year>
<Month>04</Month>
<Day>02</Day>
</DateCompleted>
<DateRevised><Year>2018</Year>
<Month>11</Month>
<Day>13</Day>
</DateRevised>
<Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">2045-2322</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>6</Volume>
<PubDate><Year>2016</Year>
<Month>05</Month>
<Day>17</Day>
</PubDate>
</JournalIssue>
<Title>Scientific reports</Title>
<ISOAbbreviation>Sci Rep</ISOAbbreviation>
</Journal>
<ArticleTitle>Induction of C/EBP homologous protein-mediated apoptosis and autophagy by licochalcone A in non-small cell lung cancer cells.</ArticleTitle>
<Pagination><MedlinePgn>26241</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1038/srep26241</ELocationID>
<Abstract><AbstractText>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.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Tang</LastName>
<ForeName>Zheng-Hai</ForeName>
<Initials>ZH</Initials>
<AffiliationInfo><Affiliation>State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao, China.</Affiliation>
</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Chen</LastName>
<ForeName>Xin</ForeName>
<Initials>X</Initials>
<AffiliationInfo><Affiliation>State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Wang</LastName>
<ForeName>Zhao-Yu</ForeName>
<Initials>ZY</Initials>
<AffiliationInfo><Affiliation>State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao, China.</Affiliation>
</AffiliationInfo>
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<ForeName>Ke</ForeName>
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<AffiliationInfo><Affiliation>State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao, China.</Affiliation>
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<ForeName>Xiao-Wen</ForeName>
<Initials>XW</Initials>
<AffiliationInfo><Affiliation>Medical Center, Yuquan Hospital, Tsinghua University, Beijing, China.</Affiliation>
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<ForeName>Jia-Hong</ForeName>
<Initials>JH</Initials>
<AffiliationInfo><Affiliation>State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao, China.</Affiliation>
</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Wang</LastName>
<ForeName>Yi-Tao</ForeName>
<Initials>YT</Initials>
<AffiliationInfo><Affiliation>State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao, China.</Affiliation>
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<ForeName>Xiu-Ping</ForeName>
<Initials>XP</Initials>
<AffiliationInfo><Affiliation>State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Lu</LastName>
<ForeName>Jin-Jian</ForeName>
<Initials>JJ</Initials>
<AffiliationInfo><Affiliation>State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao, China.</Affiliation>
</AffiliationInfo>
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<Language>eng</Language>
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<Month>05</Month>
<Day>17</Day>
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<MedlineTA>Sci Rep</MedlineTA>
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<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D047188">Chalcones</NameOfSubstance>
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<MeshHeadingList><MeshHeading><DescriptorName UI="D000072283" MajorTopicYN="N">A549 Cells</DescriptorName>
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<QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D055785" MajorTopicYN="N">Gene Knockdown Techniques</DescriptorName>
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<MeshHeading><DescriptorName UI="D029882" MajorTopicYN="N">Glycyrrhiza uralensis</DescriptorName>
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<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
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       | HfdSelect -Kh $EXPLOR_AREA/Data/Ncbi/Merge/biblio.hfd   \
       | NlmPubMed2Wicri -a ChloroquineV1

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	Serveur d'exploration Chloroquine
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Serveur d'exploration Chloroquine

Induction of C/EBP homologous protein-mediated apoptosis and autophagy by licochalcone A in non-small cell lung cancer cells.

Induction of C/EBP homologous protein-mediated apoptosis and autophagy by licochalcone A in non-small cell lung cancer cells.

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