ChloroquineV1, Main, Exploration, bibRecord, 000C57

A diphenyldiselenide derivative induces autophagy via JNK in HTB-54 lung cancer cells.

Identifieur interne : 000C57 ( Main/Exploration ); précédent : 000C56; suivant : 000C58

A diphenyldiselenide derivative induces autophagy via JNK in HTB-54 lung cancer cells.

Auteurs : Marta Díaz [Espagne] ; Roncesvalles González [Espagne] ; Daniel Plano [Espagne] ; Juan Antonio Palop [Espagne] ; Carmen Sanmartín [Espagne] ; Ignacio Encío [Espagne]

Source :

Journal of cellular and molecular medicine [ 1582-4934 ] ; 2018.

RBID : pubmed:28922542

Descripteurs français

KwdFr :
- Activation enzymatique (), Apoptose (), Autophagie (), Caspases (métabolisme), Composés organiques du sélénium (), Composés organiques du sélénium (pharmacologie), Dérivés du benzène (), Dérivés du benzène (pharmacologie), Humains, JNK Mitogen-Activated Protein Kinases (métabolisme), Lignée cellulaire tumorale, Points de contrôle du cycle cellulaire (), Tumeurs du poumon (anatomopathologie), Tumeurs du poumon (enzymologie).
MESH :
- anatomopathologie : Tumeurs du poumon.
- enzymologie : Tumeurs du poumon.
- métabolisme : Caspases, JNK Mitogen-Activated Protein Kinases.
- pharmacologie : Composés organiques du sélénium, Dérivés du benzène.
- Activation enzymatique, Apoptose, Autophagie, Composés organiques du sélénium, Dérivés du benzène, Humains, Lignée cellulaire tumorale, Points de contrôle du cycle cellulaire.

English descriptors

KwdEn :
- Apoptosis (drug effects), Autophagy (drug effects), Benzene Derivatives (chemistry), Benzene Derivatives (pharmacology), Caspases (metabolism), Cell Cycle Checkpoints (drug effects), Cell Line, Tumor, Enzyme Activation (drug effects), Humans, JNK Mitogen-Activated Protein Kinases (metabolism), Lung Neoplasms (enzymology), Lung Neoplasms (pathology), Organoselenium Compounds (chemistry), Organoselenium Compounds (pharmacology).
MESH :
- chemical , chemistry : Benzene Derivatives, Organoselenium Compounds.
- drug effects : Apoptosis, Autophagy, Cell Cycle Checkpoints, Enzyme Activation.
- enzymology : Lung Neoplasms.
- chemical , metabolism : Caspases, JNK Mitogen-Activated Protein Kinases.
- pathology : Lung Neoplasms.
- chemical , pharmacology : Benzene Derivatives, Organoselenium Compounds.
- Cell Line, Tumor, Humans.

Abstract

Symmetric aromatic diselenides are potential anticancer agents with strong cytotoxic activity. In this study, the in vitro anticancer activities of a novel series of diarylseleno derivatives from the diphenyldiselenide (DPDS) scaffold were evaluated. Most of the compounds exhibited high efficacy for inducing cytotoxicity against different human cancer cell lines. DPDS 2, the compound with the lowest mean GI₅₀ value, induced both caspase-dependent apoptosis and arrest at the G₀ /G₁ phase in acute lymphoblastic leucemia CCRF-CEM cells. Consistent with this, PARP cleavage; enhanced caspase-2, -3, -8 and -9 activity; reduced CDK4 expression and increased levels of p53 were detected in these cells upon DPDS 2 treatment. Mutated p53 expressed in CCRF-CEM cells retains its transactivating activity. Therefore, increased levels of p21^CIP1 and BAX proteins were also detected. On the other hand, DPDS 6, the compound with the highest selectivity index for cancer cells, resulted in G₂ /M cell cycle arrest and caspase-independent cell death in p53 deficient HTB-54 lung cancer cells. Autophagy inhibitors 3-methyladenine, wortmannin and chloroquine inhibited DPDS 6-induced cell death. Consistent with autophagy, increased LC3-II and decreased SQSTM1/p62 levels were detected in HTB-54 cells in response to DPDS 6. Induction of JNK phosphorylation and a reduction in phospho-p38 MAPK were also detected. Moreover, the JNK inhibitor SP600125-protected HTB-54 cells from DPDS 6-induced cell death indicating that JNK activation is involved in DPDS 6-induced autophagy. These results highlight the anticancer effects of these derivatives and warrant future studies examining their clinical potential.

DOI: 10.1111/jcmm.13318
PubMed: 28922542

Affiliations:

Espagne

Le document en format XML

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<author><name sortKey="Diaz, Marta" sort="Diaz, Marta" uniqKey="Diaz M" first="Marta" last="Díaz">Marta Díaz</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Organic and Pharmaceutical Chemistry, Faculty of Pharmacy and Nutrition, University of Navarra, Pamplona, Spain.</nlm:affiliation>
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<author><name sortKey="Palop, Juan Antonio" sort="Palop, Juan Antonio" uniqKey="Palop J" first="Juan Antonio" last="Palop">Juan Antonio Palop</name>
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<term>Autophagy (drug effects)</term>
<term>Benzene Derivatives (chemistry)</term>
<term>Benzene Derivatives (pharmacology)</term>
<term>Caspases (metabolism)</term>
<term>Cell Cycle Checkpoints (drug effects)</term>
<term>Cell Line, Tumor</term>
<term>Enzyme Activation (drug effects)</term>
<term>Humans</term>
<term>JNK Mitogen-Activated Protein Kinases (metabolism)</term>
<term>Lung Neoplasms (enzymology)</term>
<term>Lung Neoplasms (pathology)</term>
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<term>Organoselenium Compounds (pharmacology)</term>
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<keywords scheme="KwdFr" xml:lang="fr"><term>Activation enzymatique ()</term>
<term>Apoptose ()</term>
<term>Autophagie ()</term>
<term>Caspases (métabolisme)</term>
<term>Composés organiques du sélénium ()</term>
<term>Composés organiques du sélénium (pharmacologie)</term>
<term>Dérivés du benzène ()</term>
<term>Dérivés du benzène (pharmacologie)</term>
<term>Humains</term>
<term>JNK Mitogen-Activated Protein Kinases (métabolisme)</term>
<term>Lignée cellulaire tumorale</term>
<term>Points de contrôle du cycle cellulaire ()</term>
<term>Tumeurs du poumon (anatomopathologie)</term>
<term>Tumeurs du poumon (enzymologie)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="chemistry" xml:lang="en"><term>Benzene Derivatives</term>
<term>Organoselenium Compounds</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 Cycle Checkpoints</term>
<term>Enzyme Activation</term>
</keywords>
<keywords scheme="MESH" qualifier="enzymologie" xml:lang="fr"><term>Tumeurs du poumon</term>
</keywords>
<keywords scheme="MESH" qualifier="enzymology" xml:lang="en"><term>Lung Neoplasms</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Caspases</term>
<term>JNK Mitogen-Activated Protein Kinases</term>
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<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Caspases</term>
<term>JNK Mitogen-Activated Protein Kinases</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Lung Neoplasms</term>
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<keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Composés organiques du sélénium</term>
<term>Dérivés du benzène</term>
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<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Benzene Derivatives</term>
<term>Organoselenium Compounds</term>
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<term>Humans</term>
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<term>Apoptose</term>
<term>Autophagie</term>
<term>Composés organiques du sélénium</term>
<term>Dérivés du benzène</term>
<term>Humains</term>
<term>Lignée cellulaire tumorale</term>
<term>Points de contrôle du cycle cellulaire</term>
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<front><div type="abstract" xml:lang="en">Symmetric aromatic diselenides are potential anticancer agents with strong cytotoxic activity. In this study, the in vitro anticancer activities of a novel series of diarylseleno derivatives from the diphenyldiselenide (DPDS) scaffold were evaluated. Most of the compounds exhibited high efficacy for inducing cytotoxicity against different human cancer cell lines. DPDS 2, the compound with the lowest mean GI<sub>50</sub>
 value, induced both caspase-dependent apoptosis and arrest at the G<sub>0</sub>
 /G<sub>1</sub>
 phase in acute lymphoblastic leucemia CCRF-CEM cells. Consistent with this, PARP cleavage; enhanced caspase-2, -3, -8 and -9 activity; reduced CDK4 expression and increased levels of p53 were detected in these cells upon DPDS 2 treatment. Mutated p53 expressed in CCRF-CEM cells retains its transactivating activity. Therefore, increased levels of p21<sup>CIP1</sup>
 and BAX proteins were also detected. On the other hand, DPDS 6, the compound with the highest selectivity index for cancer cells, resulted in G<sub>2</sub>
 /M cell cycle arrest and caspase-independent cell death in p53 deficient HTB-54 lung cancer cells. Autophagy inhibitors 3-methyladenine, wortmannin and chloroquine inhibited DPDS 6-induced cell death. Consistent with autophagy, increased LC3-II and decreased SQSTM1/p62 levels were detected in HTB-54 cells in response to DPDS 6. Induction of JNK phosphorylation and a reduction in phospho-p38 MAPK were also detected. Moreover, the JNK inhibitor SP600125-protected HTB-54 cells from DPDS 6-induced cell death indicating that JNK activation is involved in DPDS 6-induced autophagy. These results highlight the anticancer effects of these derivatives and warrant future studies examining their clinical potential.</div>
</front>
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<tree><country name="Espagne"><noRegion><name sortKey="Diaz, Marta" sort="Diaz, Marta" uniqKey="Diaz M" first="Marta" last="Díaz">Marta Díaz</name>
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<name sortKey="Encio, Ignacio" sort="Encio, Ignacio" uniqKey="Encio I" first="Ignacio" last="Encío">Ignacio Encío</name>
<name sortKey="Gonzalez, Roncesvalles" sort="Gonzalez, Roncesvalles" uniqKey="Gonzalez R" first="Roncesvalles" last="González">Roncesvalles González</name>
<name sortKey="Palop, Juan Antonio" sort="Palop, Juan Antonio" uniqKey="Palop J" first="Juan Antonio" last="Palop">Juan Antonio Palop</name>
<name sortKey="Plano, Daniel" sort="Plano, Daniel" uniqKey="Plano D" first="Daniel" last="Plano">Daniel Plano</name>
<name sortKey="Sanmartin, Carmen" sort="Sanmartin, Carmen" uniqKey="Sanmartin C" first="Carmen" last="Sanmartín">Carmen Sanmartín</name>
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Serveur d'exploration Chloroquine

A diphenyldiselenide derivative induces autophagy via JNK in HTB-54 lung cancer cells.

A diphenyldiselenide derivative induces autophagy via JNK in HTB-54 lung cancer cells.

Source :

Descripteurs français

English descriptors

Abstract

Links toward previous steps (curation, corpus...)

Le document en format XML

Pour manipuler ce document sous Unix (Dilib)

Pour mettre un lien sur cette page dans le réseau Wicri

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