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

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...

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Autores: Diaz, M. (Marta)|||/items/cde81b70-e69d-433e-aabc-cf4dbecff8ba, González, R. (Roncesvalles)|||/items/0fd6fddd-3be4-4b17-9ecd-5c0d1f7811d9, Plano-Amatriain, D. (Daniel)|||/items/238881e4-7d5e-4598-924d-4392e3b7e02e, Palop-Cubillo, J.A. (Juan Antonio)|||/items/bfa23090-c589-4aeb-89e5-bbe9aa243a90, Sanmartin-Grijalba, C. (Carmen)|||/items/d36bd105-ab64-427d-9745-5812cf5e7af7, Encío-Martínez, I.J. (Ignacio José)|||/items/468e76be-1795-41af-a6a3-f7c4472e416c
Tipo de recurso: artículo
Fecha de publicación:2018
País:España
Institución:Universidad de Navarra
Repositorio:Dadun. Depósito Académico Digital de la Universidad de Navarra
Idioma:inglés
OAI Identifier:oai:dadun.unav.edu:10171/64738
Acceso en línea:https://hdl.handle.net/10171/64738
Access Level:acceso abierto
Palabra clave:p53
p38 MAPK
JNK
Diphenyldiselenide
Autophagy
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spelling A diphenyldiselenide derivative induces autophagy via JNK in HTB-54 lung cancer cellsDiaz, M. (Marta)|||/items/cde81b70-e69d-433e-aabc-cf4dbecff8baGonzález, R. (Roncesvalles)|||/items/0fd6fddd-3be4-4b17-9ecd-5c0d1f7811d9Plano-Amatriain, D. (Daniel)|||/items/238881e4-7d5e-4598-924d-4392e3b7e02ePalop-Cubillo, J.A. (Juan Antonio)|||/items/bfa23090-c589-4aeb-89e5-bbe9aa243a90Sanmartin-Grijalba, C. (Carmen)|||/items/d36bd105-ab64-427d-9745-5812cf5e7af7Encío-Martínez, I.J. (Ignacio José)|||/items/468e76be-1795-41af-a6a3-f7c4472e416cp53p38 MAPKJNKDiphenyldiselenideAutophagySymmetric 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 p21CIP1 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.WileyDadun. Depósito Académico Digital Universidad de Navarra20222022-11-3020182018-01-0120182018-01-01journal articlehttp://purl.org/coar/resource_type/c_6501info:eu-repo/semantics/articleapplication/pdfhttps://hdl.handle.net/10171/64738reponame:Dadun. Depósito Académico Digital de la Universidad de Navarrainstname:Universidad de NavarraInglésengopen accesshttp://purl.org/coar/access_right/c_abf2info:eu-repo/semantics/openAccessoai:dadun.unav.edu:10171/647382026-06-21T12:47:57Z
dc.title.none.fl_str_mv A diphenyldiselenide derivative induces autophagy via JNK in HTB-54 lung cancer cells
title A diphenyldiselenide derivative induces autophagy via JNK in HTB-54 lung cancer cells
spellingShingle A diphenyldiselenide derivative induces autophagy via JNK in HTB-54 lung cancer cells
Diaz, M. (Marta)|||/items/cde81b70-e69d-433e-aabc-cf4dbecff8ba
p53
p38 MAPK
JNK
Diphenyldiselenide
Autophagy
title_short A diphenyldiselenide derivative induces autophagy via JNK in HTB-54 lung cancer cells
title_full A diphenyldiselenide derivative induces autophagy via JNK in HTB-54 lung cancer cells
title_fullStr A diphenyldiselenide derivative induces autophagy via JNK in HTB-54 lung cancer cells
title_full_unstemmed A diphenyldiselenide derivative induces autophagy via JNK in HTB-54 lung cancer cells
title_sort A diphenyldiselenide derivative induces autophagy via JNK in HTB-54 lung cancer cells
dc.creator.none.fl_str_mv Diaz, M. (Marta)|||/items/cde81b70-e69d-433e-aabc-cf4dbecff8ba
González, R. (Roncesvalles)|||/items/0fd6fddd-3be4-4b17-9ecd-5c0d1f7811d9
Plano-Amatriain, D. (Daniel)|||/items/238881e4-7d5e-4598-924d-4392e3b7e02e
Palop-Cubillo, J.A. (Juan Antonio)|||/items/bfa23090-c589-4aeb-89e5-bbe9aa243a90
Sanmartin-Grijalba, C. (Carmen)|||/items/d36bd105-ab64-427d-9745-5812cf5e7af7
Encío-Martínez, I.J. (Ignacio José)|||/items/468e76be-1795-41af-a6a3-f7c4472e416c
author Diaz, M. (Marta)|||/items/cde81b70-e69d-433e-aabc-cf4dbecff8ba
author_facet Diaz, M. (Marta)|||/items/cde81b70-e69d-433e-aabc-cf4dbecff8ba
González, R. (Roncesvalles)|||/items/0fd6fddd-3be4-4b17-9ecd-5c0d1f7811d9
Plano-Amatriain, D. (Daniel)|||/items/238881e4-7d5e-4598-924d-4392e3b7e02e
Palop-Cubillo, J.A. (Juan Antonio)|||/items/bfa23090-c589-4aeb-89e5-bbe9aa243a90
Sanmartin-Grijalba, C. (Carmen)|||/items/d36bd105-ab64-427d-9745-5812cf5e7af7
Encío-Martínez, I.J. (Ignacio José)|||/items/468e76be-1795-41af-a6a3-f7c4472e416c
author_role author
author2 González, R. (Roncesvalles)|||/items/0fd6fddd-3be4-4b17-9ecd-5c0d1f7811d9
Plano-Amatriain, D. (Daniel)|||/items/238881e4-7d5e-4598-924d-4392e3b7e02e
Palop-Cubillo, J.A. (Juan Antonio)|||/items/bfa23090-c589-4aeb-89e5-bbe9aa243a90
Sanmartin-Grijalba, C. (Carmen)|||/items/d36bd105-ab64-427d-9745-5812cf5e7af7
Encío-Martínez, I.J. (Ignacio José)|||/items/468e76be-1795-41af-a6a3-f7c4472e416c
author2_role author
author
author
author
author
dc.contributor.none.fl_str_mv Dadun. Depósito Académico Digital Universidad de Navarra
dc.subject.none.fl_str_mv p53
p38 MAPK
JNK
Diphenyldiselenide
Autophagy
topic p53
p38 MAPK
JNK
Diphenyldiselenide
Autophagy
description 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 p21CIP1 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.
publishDate 2018
dc.date.none.fl_str_mv 2018
2018-01-01
2018
2018-01-01
2022
2022-11-30
dc.type.none.fl_str_mv journal article
http://purl.org/coar/resource_type/c_6501
dc.type.openaire.fl_str_mv info:eu-repo/semantics/article
format article
dc.identifier.none.fl_str_mv https://hdl.handle.net/10171/64738
url https://hdl.handle.net/10171/64738
dc.language.none.fl_str_mv Inglés
eng
language_invalid_str_mv Inglés
language eng
dc.rights.none.fl_str_mv open access
http://purl.org/coar/access_right/c_abf2
dc.rights.openaire.fl_str_mv info:eu-repo/semantics/openAccess
rights_invalid_str_mv open access
http://purl.org/coar/access_right/c_abf2
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv application/pdf
dc.publisher.none.fl_str_mv Wiley
publisher.none.fl_str_mv Wiley
dc.source.none.fl_str_mv reponame:Dadun. Depósito Académico Digital de la Universidad de Navarra
instname:Universidad de Navarra
instname_str Universidad de Navarra
reponame_str Dadun. Depósito Académico Digital de la Universidad de Navarra
collection Dadun. Depósito Académico Digital de la Universidad de Navarra
repository.name.fl_str_mv
repository.mail.fl_str_mv
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