Cucurbitacin E induces caspase-dependent apoptosis and protective autophagy mediated by ROS in lung cancer cells.
Identifieur interne : 000D73 ( Main/Exploration ); précédent : 000D72; suivant : 000D74Cucurbitacin E induces caspase-dependent apoptosis and protective autophagy mediated by ROS in lung cancer cells.
Auteurs : Guixin Ma ; Weiwei Luo ; Jinjian Lu ; Dik-Lung Ma [Hong Kong] ; Chung-Hang Leung ; Yitao Wang ; Xiuping ChenSource :
- Chemico-biological interactions [ 1872-7786 ] ; 2016.
Descripteurs français
- KwdFr :
- Acétylcystéine (pharmacologie), Apoptose (), Autophagie (), Caspase-3 (métabolisme), Caspase-7 (métabolisme), Chloroquine (toxicité), Espèces réactives de l'oxygène (métabolisme), Humains, Lignée cellulaire tumorale, Macrolides (toxicité), Microscopie de fluorescence, Poly(ADP-ribose) polymerases (métabolisme), Potentiel de membrane mitochondriale (), Prolifération cellulaire (), Protéines associées aux microtubules (métabolisme), Protéines proto-oncogènes c-bcl-2 (métabolisme), Synergie des médicaments, Technique de Western, Triterpènes (toxicité), Tumeurs du poumon (anatomopathologie), Tumeurs du poumon (métabolisme).
- MESH :
- anatomopathologie : Tumeurs du poumon.
- métabolisme : Caspase-3, Caspase-7, Espèces réactives de l'oxygène, Poly(ADP-ribose) polymerases, Protéines associées aux microtubules, Protéines proto-oncogènes c-bcl-2, Tumeurs du poumon.
- pharmacologie : Acétylcystéine.
- toxicité : Chloroquine, Macrolides, Triterpènes.
- Apoptose, Autophagie, Humains, Lignée cellulaire tumorale, Microscopie de fluorescence, Potentiel de membrane mitochondriale, Prolifération cellulaire, Synergie des médicaments, Technique de Western.
English descriptors
- KwdEn :
- Acetylcysteine (pharmacology), Apoptosis (drug effects), Autophagy (drug effects), Blotting, Western, Caspase 3 (metabolism), Caspase 7 (metabolism), Cell Line, Tumor, Cell Proliferation (drug effects), Chloroquine (toxicity), Drug Synergism, Humans, Lung Neoplasms (metabolism), Lung Neoplasms (pathology), Macrolides (toxicity), Membrane Potential, Mitochondrial (drug effects), Microscopy, Fluorescence, Microtubule-Associated Proteins (metabolism), Poly(ADP-ribose) Polymerases (metabolism), Proto-Oncogene Proteins c-bcl-2 (metabolism), Reactive Oxygen Species (metabolism), Triterpenes (toxicity).
- MESH :
- chemical , metabolism : Caspase 3, Caspase 7, Microtubule-Associated Proteins, Poly(ADP-ribose) Polymerases, Proto-Oncogene Proteins c-bcl-2, Reactive Oxygen Species.
- chemical , pharmacology : Acetylcysteine.
- drug effects : Apoptosis, Autophagy, Cell Proliferation, Membrane Potential, Mitochondrial.
- metabolism : Lung Neoplasms.
- pathology : Lung Neoplasms.
- chemical , toxicity : Chloroquine, Macrolides, Triterpenes.
- Blotting, Western, Cell Line, Tumor, Drug Synergism, Humans, Microscopy, Fluorescence.
Abstract
Cucurbitacin E (CuE) is a triterpenoid with potent anticancer activities while the underlying mechanisms remain elusive. In the present study, the anticancer effects of CuE on 95D lung cancer cells were investigated. CuE decreased cell viability, inhibited colony formation, and increased reactive oxygen species (ROS) in a concentration-dependent manner, which were reversed by N-acetyl-l-cysteine (NAC). CuE induced apoptosis as determined by JC-1 staining, expression of Bcl-2 family proteins, cleavage of caspases, and TUNEL staining. NAC and Ac-DEVD-CHO partially reversed CuE-induced cleavage of caspase-3, caspase-7, and PARP. Furthermore, CuE caused accumulation of autophagic vacuoles and concentration- and time-dependent expression of LC3II protein. Autophagy inhibitors chloroquine and bafilomycin A1 enhanced CuE-induced LC3II expression and cell death. CuE-triggered protein expression of p-AKT, p-mTOR, Beclin-1, and p-ULK1 was partially reversed by NAC pretreatment. In addition, CuE treatment damaged F-actin without affecting β-tubulin as confirmed by immunofluorescence. In conclusion, CuE induced ROS-dependent apoptosis through Bcl-2 family and caspases in 95D lung cancer cells. Furthermore, CuE induced protective autophagy mediated by ROS through AKT/mTOR pathway. This study provides novel roles of ROS in the anticancer effect of CuE.
DOI: 10.1016/j.cbi.2016.04.028
PubMed: 27106530
Affiliations:
Links toward previous steps (curation, corpus...)
- to stream PubMed, to step Corpus: 000209
- to stream PubMed, to step Curation: 000209
- to stream PubMed, to step Checkpoint: 000208
- to stream Ncbi, to step Merge: 000338
- to stream Ncbi, to step Curation: 000338
- to stream Ncbi, to step Checkpoint: 000338
- to stream Main, to step Merge: 000D74
- to stream Main, to step Curation: 000D73
Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Cucurbitacin E induces caspase-dependent apoptosis and protective autophagy mediated by ROS in lung cancer cells.</title><author><name sortKey="Ma, Guixin" sort="Ma, Guixin" uniqKey="Ma G" first="Guixin" last="Ma">Guixin Ma</name><affiliation><nlm:affiliation>State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao.</nlm:affiliation><wicri:noCountry code="subField">Macao</wicri:noCountry></affiliation></author><author><name sortKey="Luo, Weiwei" sort="Luo, Weiwei" uniqKey="Luo W" first="Weiwei" last="Luo">Weiwei Luo</name><affiliation><nlm:affiliation>State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao.</nlm:affiliation><wicri:noCountry code="subField">Macao</wicri:noCountry></affiliation></author><author><name sortKey="Lu, Jinjian" sort="Lu, Jinjian" uniqKey="Lu J" first="Jinjian" last="Lu">Jinjian Lu</name><affiliation><nlm:affiliation>State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao.</nlm:affiliation><wicri:noCountry code="subField">Macao</wicri:noCountry></affiliation></author><author><name sortKey="Ma, Dik Lung" sort="Ma, Dik Lung" uniqKey="Ma D" first="Dik-Lung" last="Ma">Dik-Lung Ma</name><affiliation wicri:level="1"><nlm:affiliation>Department of Chemistry, Hong Kong Baptist University, Kowloon Tong, Hong Kong.</nlm:affiliation><country xml:lang="fr">Hong Kong</country><wicri:regionArea>Department of Chemistry, Hong Kong Baptist University, Kowloon Tong</wicri:regionArea><wicri:noRegion>Kowloon Tong</wicri:noRegion></affiliation></author><author><name sortKey="Leung, Chung Hang" sort="Leung, Chung Hang" uniqKey="Leung C" first="Chung-Hang" last="Leung">Chung-Hang Leung</name><affiliation><nlm:affiliation>State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao.</nlm:affiliation><wicri:noCountry code="subField">Macao</wicri:noCountry></affiliation></author><author><name sortKey="Wang, Yitao" sort="Wang, Yitao" uniqKey="Wang Y" first="Yitao" last="Wang">Yitao Wang</name><affiliation><nlm:affiliation>State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao.</nlm:affiliation><wicri:noCountry code="subField">Macao</wicri:noCountry></affiliation></author><author><name sortKey="Chen, Xiuping" sort="Chen, Xiuping" uniqKey="Chen X" first="Xiuping" last="Chen">Xiuping Chen</name><affiliation><nlm:affiliation>State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao. Electronic address: xpchen@umac.mo.</nlm:affiliation><wicri:noCountry code="subField">Macao</wicri:noCountry></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2016">2016</date><idno type="RBID">pubmed:27106530</idno><idno type="pmid">27106530</idno><idno type="doi">10.1016/j.cbi.2016.04.028</idno><idno type="wicri:Area/PubMed/Corpus">000209</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000209</idno><idno type="wicri:Area/PubMed/Curation">000209</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">000209</idno><idno type="wicri:Area/PubMed/Checkpoint">000208</idno><idno type="wicri:explorRef" wicri:stream="Checkpoint" wicri:step="PubMed">000208</idno><idno type="wicri:Area/Ncbi/Merge">000338</idno><idno type="wicri:Area/Ncbi/Curation">000338</idno><idno type="wicri:Area/Ncbi/Checkpoint">000338</idno><idno type="wicri:Area/Main/Merge">000D74</idno><idno type="wicri:Area/Main/Curation">000D73</idno><idno type="wicri:Area/Main/Exploration">000D73</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Cucurbitacin E induces caspase-dependent apoptosis and protective autophagy mediated by ROS in lung cancer cells.</title><author><name sortKey="Ma, Guixin" sort="Ma, Guixin" uniqKey="Ma G" first="Guixin" last="Ma">Guixin Ma</name><affiliation><nlm:affiliation>State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao.</nlm:affiliation><wicri:noCountry code="subField">Macao</wicri:noCountry></affiliation></author><author><name sortKey="Luo, Weiwei" sort="Luo, Weiwei" uniqKey="Luo W" first="Weiwei" last="Luo">Weiwei Luo</name><affiliation><nlm:affiliation>State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao.</nlm:affiliation><wicri:noCountry code="subField">Macao</wicri:noCountry></affiliation></author><author><name sortKey="Lu, Jinjian" sort="Lu, Jinjian" uniqKey="Lu J" first="Jinjian" last="Lu">Jinjian Lu</name><affiliation><nlm:affiliation>State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao.</nlm:affiliation><wicri:noCountry code="subField">Macao</wicri:noCountry></affiliation></author><author><name sortKey="Ma, Dik Lung" sort="Ma, Dik Lung" uniqKey="Ma D" first="Dik-Lung" last="Ma">Dik-Lung Ma</name><affiliation wicri:level="1"><nlm:affiliation>Department of Chemistry, Hong Kong Baptist University, Kowloon Tong, Hong Kong.</nlm:affiliation><country xml:lang="fr">Hong Kong</country><wicri:regionArea>Department of Chemistry, Hong Kong Baptist University, Kowloon Tong</wicri:regionArea><wicri:noRegion>Kowloon Tong</wicri:noRegion></affiliation></author><author><name sortKey="Leung, Chung Hang" sort="Leung, Chung Hang" uniqKey="Leung C" first="Chung-Hang" last="Leung">Chung-Hang Leung</name><affiliation><nlm:affiliation>State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao.</nlm:affiliation><wicri:noCountry code="subField">Macao</wicri:noCountry></affiliation></author><author><name sortKey="Wang, Yitao" sort="Wang, Yitao" uniqKey="Wang Y" first="Yitao" last="Wang">Yitao Wang</name><affiliation><nlm:affiliation>State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao.</nlm:affiliation><wicri:noCountry code="subField">Macao</wicri:noCountry></affiliation></author><author><name sortKey="Chen, Xiuping" sort="Chen, Xiuping" uniqKey="Chen X" first="Xiuping" last="Chen">Xiuping Chen</name><affiliation><nlm:affiliation>State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao. Electronic address: xpchen@umac.mo.</nlm:affiliation><wicri:noCountry code="subField">Macao</wicri:noCountry></affiliation></author></analytic><series><title level="j">Chemico-biological interactions</title><idno type="eISSN">1872-7786</idno><imprint><date when="2016" type="published">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Acetylcysteine (pharmacology)</term><term>Apoptosis (drug effects)</term><term>Autophagy (drug effects)</term><term>Blotting, Western</term><term>Caspase 3 (metabolism)</term><term>Caspase 7 (metabolism)</term><term>Cell Line, Tumor</term><term>Cell Proliferation (drug effects)</term><term>Chloroquine (toxicity)</term><term>Drug Synergism</term><term>Humans</term><term>Lung Neoplasms (metabolism)</term><term>Lung Neoplasms (pathology)</term><term>Macrolides (toxicity)</term><term>Membrane Potential, Mitochondrial (drug effects)</term><term>Microscopy, Fluorescence</term><term>Microtubule-Associated Proteins (metabolism)</term><term>Poly(ADP-ribose) Polymerases (metabolism)</term><term>Proto-Oncogene Proteins c-bcl-2 (metabolism)</term><term>Reactive Oxygen Species (metabolism)</term><term>Triterpenes (toxicity)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Acétylcystéine (pharmacologie)</term><term>Apoptose ()</term><term>Autophagie ()</term><term>Caspase-3 (métabolisme)</term><term>Caspase-7 (métabolisme)</term><term>Chloroquine (toxicité)</term><term>Espèces réactives de l'oxygène (métabolisme)</term><term>Humains</term><term>Lignée cellulaire tumorale</term><term>Macrolides (toxicité)</term><term>Microscopie de fluorescence</term><term>Poly(ADP-ribose) polymerases (métabolisme)</term><term>Potentiel de membrane mitochondriale ()</term><term>Prolifération cellulaire ()</term><term>Protéines associées aux microtubules (métabolisme)</term><term>Protéines proto-oncogènes c-bcl-2 (métabolisme)</term><term>Synergie des médicaments</term><term>Technique de Western</term><term>Triterpènes (toxicité)</term><term>Tumeurs du poumon (anatomopathologie)</term><term>Tumeurs du poumon (métabolisme)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Caspase 3</term><term>Caspase 7</term><term>Microtubule-Associated Proteins</term><term>Poly(ADP-ribose) Polymerases</term><term>Proto-Oncogene Proteins c-bcl-2</term><term>Reactive Oxygen Species</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Acetylcysteine</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Tumeurs du poumon</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Apoptosis</term><term>Autophagy</term><term>Cell Proliferation</term><term>Membrane Potential, Mitochondrial</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Lung Neoplasms</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Caspase-3</term><term>Caspase-7</term><term>Espèces réactives de l'oxygène</term><term>Poly(ADP-ribose) polymerases</term><term>Protéines associées aux microtubules</term><term>Protéines proto-oncogènes c-bcl-2</term><term>Tumeurs du poumon</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Lung Neoplasms</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Acétylcystéine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="toxicity" xml:lang="en"><term>Chloroquine</term><term>Macrolides</term><term>Triterpenes</term></keywords><keywords scheme="MESH" qualifier="toxicité" xml:lang="fr"><term>Chloroquine</term><term>Macrolides</term><term>Triterpènes</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Blotting, Western</term><term>Cell Line, Tumor</term><term>Drug Synergism</term><term>Humans</term><term>Microscopy, Fluorescence</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Apoptose</term><term>Autophagie</term><term>Humains</term><term>Lignée cellulaire tumorale</term><term>Microscopie de fluorescence</term><term>Potentiel de membrane mitochondriale</term><term>Prolifération cellulaire</term><term>Synergie des médicaments</term><term>Technique de Western</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Cucurbitacin E (CuE) is a triterpenoid with potent anticancer activities while the underlying mechanisms remain elusive. In the present study, the anticancer effects of CuE on 95D lung cancer cells were investigated. CuE decreased cell viability, inhibited colony formation, and increased reactive oxygen species (ROS) in a concentration-dependent manner, which were reversed by N-acetyl-l-cysteine (NAC). CuE induced apoptosis as determined by JC-1 staining, expression of Bcl-2 family proteins, cleavage of caspases, and TUNEL staining. NAC and Ac-DEVD-CHO partially reversed CuE-induced cleavage of caspase-3, caspase-7, and PARP. Furthermore, CuE caused accumulation of autophagic vacuoles and concentration- and time-dependent expression of LC3II protein. Autophagy inhibitors chloroquine and bafilomycin A1 enhanced CuE-induced LC3II expression and cell death. CuE-triggered protein expression of p-AKT, p-mTOR, Beclin-1, and p-ULK1 was partially reversed by NAC pretreatment. In addition, CuE treatment damaged F-actin without affecting β-tubulin as confirmed by immunofluorescence. In conclusion, CuE induced ROS-dependent apoptosis through Bcl-2 family and caspases in 95D lung cancer cells. Furthermore, CuE induced protective autophagy mediated by ROS through AKT/mTOR pathway. This study provides novel roles of ROS in the anticancer effect of CuE. </div></front></TEI><affiliations><list><country><li>Hong Kong</li></country></list><tree><noCountry><name sortKey="Chen, Xiuping" sort="Chen, Xiuping" uniqKey="Chen X" first="Xiuping" last="Chen">Xiuping Chen</name><name sortKey="Leung, Chung Hang" sort="Leung, Chung Hang" uniqKey="Leung C" first="Chung-Hang" last="Leung">Chung-Hang Leung</name><name sortKey="Lu, Jinjian" sort="Lu, Jinjian" uniqKey="Lu J" first="Jinjian" last="Lu">Jinjian Lu</name><name sortKey="Luo, Weiwei" sort="Luo, Weiwei" uniqKey="Luo W" first="Weiwei" last="Luo">Weiwei Luo</name><name sortKey="Ma, Guixin" sort="Ma, Guixin" uniqKey="Ma G" first="Guixin" last="Ma">Guixin Ma</name><name sortKey="Wang, Yitao" sort="Wang, Yitao" uniqKey="Wang Y" first="Yitao" last="Wang">Yitao Wang</name></noCountry><country name="Hong Kong"><noRegion><name sortKey="Ma, Dik Lung" sort="Ma, Dik Lung" uniqKey="Ma D" first="Dik-Lung" last="Ma">Dik-Lung Ma</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Sante/explor/ChloroquineV1/Data/Main/Exploration
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000D73 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd -nk 000D73 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Sante
|area= ChloroquineV1
|flux= Main
|étape= Exploration
|type= RBID
|clé= pubmed:27106530
|texte= Cucurbitacin E induces caspase-dependent apoptosis and protective autophagy mediated by ROS in lung cancer cells.
}}
Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/Main/Exploration/RBID.i -Sk "pubmed:27106530" \
| HfdSelect -Kh $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd \
| NlmPubMed2Wicri -a ChloroquineV1
| This area was generated with Dilib version V0.6.33. |  |