Decoding the anticancer activity of VO-clioquinol compound: the mechanism of action and cell death pathways in human osteosarcoma cells

Autores
León, Ignacio Esteban; Díez, Paula; Baran, Enrique José; Etcheverry, Susana Beatriz; Fuentes, Manuel
Año de publicación
2017
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Vanadium compounds were studied in recent years by considering them as a representative of a new class of non-platinum metal anticancer drugs. However, a few challenges still remain in the discovery of new molecular targets of these new metallodrugs. Studies on cell signaling pathways related to vanadium compounds have scarcely been reported and so far this information is highly critical for identifying novel targets that play a key role in the antitumor actions of vanadium complexes. This research deals with the alterations in the intracellular signaling pathways promoted by an oxovanadium(IV) complex with the clioquinol (5-chloro-7-iodo-8-quinolinol), VO(CQ)2, on a human osteosarcoma cell line (MG-63). Herein are reported, for the first time, the antitumor properties of VO(CQ)2 and the relative abundance of 224 proteins (which are involved in most of the common intracellular pathways) to identify novel targets of the studied complex. Besides, full-length human recombinant AKT1 kinase was produced by using an IVTT system to evaluate the variation of relative tyrosin-phosphorylation levels caused by this compound. The results of the differential protein expression levels reveal several up-regulated proteins such as CASP3, CASP6, CASP7, CASP10, CASP11, Bcl-x, DAPK and down-regulated ones, such as PKB/AKT, DIABLO, among others. Moreover, cell signaling pathways involved in several altered pathways related to the PKC and AP2 family have been identified in both treatments (2.5 and 10 μM) suggesting the crucial antitumoral role of VO(CQ)2. Finally, it has been demonstrated that this compound (10 μM, 6 h) triggers a decrease of 2-fold in in situ AKT1 expression.
Puede accederse a los datos primarios de este trabajo haciendo clic en "Documentos relacionados".
Facultad de Ciencias Exactas
Centro de Química Inorgánica
Materia
Ciencias Exactas
Química
Ciencias Médicas
vanadium
AKT
cancer
Osteosarcoma
Nivel de accesibilidad
acceso abierto
Condiciones de uso
http://creativecommons.org/licenses/by-nc-sa/4.0/
Repositorio
SEDICI (UNLP)
Institución
Universidad Nacional de La Plata
OAI Identificador
oai:sedici.unlp.edu.ar:10915/108044
Acceder
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network_name_str SEDICI (UNLP)
spelling Decoding the anticancer activity of VO-clioquinol compound: the mechanism of action and cell death pathways in human osteosarcoma cellsLeón, Ignacio EstebanDíez, PaulaBaran, Enrique JoséEtcheverry, Susana BeatrizFuentes, ManuelCiencias ExactasQuímicaCiencias MédicasvanadiumAKTcancerOsteosarcomaVanadium compounds were studied in recent years by considering them as a representative of a new class of non-platinum metal anticancer drugs. However, a few challenges still remain in the discovery of new molecular targets of these new metallodrugs. Studies on cell signaling pathways related to vanadium compounds have scarcely been reported and so far this information is highly critical for identifying novel targets that play a key role in the antitumor actions of vanadium complexes. This research deals with the alterations in the intracellular signaling pathways promoted by an oxovanadium(IV) complex with the clioquinol (5-chloro-7-iodo-8-quinolinol), VO(CQ)<sub>2</sub>, on a human osteosarcoma cell line (MG-63). Herein are reported, for the first time, the antitumor properties of VO(CQ)<sub>2</sub> and the relative abundance of 224 proteins (which are involved in most of the common intracellular pathways) to identify novel targets of the studied complex. Besides, full-length human recombinant AKT1 kinase was produced by using an IVTT system to evaluate the variation of relative tyrosin-phosphorylation levels caused by this compound. The results of the differential protein expression levels reveal several up-regulated proteins such as CASP3, CASP6, CASP7, CASP10, CASP11, Bcl-x, DAPK and down-regulated ones, such as PKB/AKT, DIABLO, among others. Moreover, cell signaling pathways involved in several altered pathways related to the PKC and AP2 family have been identified in both treatments (2.5 and 10 μM) suggesting the crucial antitumoral role of VO(CQ)<sub>2</sub>. Finally, it has been demonstrated that this compound (10 μM, 6 h) triggers a decrease of 2-fold in <i>in situ</i> AKT1 expression.Puede accederse a los datos primarios de este trabajo haciendo clic en "Documentos relacionados".Facultad de Ciencias ExactasCentro de Química Inorgánica2017info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionArticulohttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdf891-901http://sedici.unlp.edu.ar/handle/10915/108044enginfo:eu-repo/semantics/altIdentifier/url/https://pubs.rsc.org/en/content/articlelanding/2017/MT/C7MT00068Einfo:eu-repo/semantics/altIdentifier/issn/1756-591Xinfo:eu-repo/semantics/altIdentifier/doi/10.1039/c7mt00068einfo:eu-repo/semantics/reference/hdl/10915/108112info:eu-repo/semantics/openAccesshttp://creativecommons.org/licenses/by-nc-sa/4.0/Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0)reponame:SEDICI (UNLP)instname:Universidad Nacional de La Platainstacron:UNLP2025-09-29T11:24:27Zoai:sedici.unlp.edu.ar:10915/108044Institucionalhttp://sedici.unlp.edu.ar/Universidad públicaNo correspondehttp://sedici.unlp.edu.ar/oai/snrdalira@sedici.unlp.edu.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:13292025-09-29 11:24:27.762SEDICI (UNLP) - Universidad Nacional de La Platafalse
dc.title.none.fl_str_mv Decoding the anticancer activity of VO-clioquinol compound: the mechanism of action and cell death pathways in human osteosarcoma cells
title Decoding the anticancer activity of VO-clioquinol compound: the mechanism of action and cell death pathways in human osteosarcoma cells
spellingShingle Decoding the anticancer activity of VO-clioquinol compound: the mechanism of action and cell death pathways in human osteosarcoma cells
León, Ignacio Esteban
Ciencias Exactas
Química
Ciencias Médicas
vanadium
AKT
cancer
Osteosarcoma
title_short Decoding the anticancer activity of VO-clioquinol compound: the mechanism of action and cell death pathways in human osteosarcoma cells
title_full Decoding the anticancer activity of VO-clioquinol compound: the mechanism of action and cell death pathways in human osteosarcoma cells
title_fullStr Decoding the anticancer activity of VO-clioquinol compound: the mechanism of action and cell death pathways in human osteosarcoma cells
title_full_unstemmed Decoding the anticancer activity of VO-clioquinol compound: the mechanism of action and cell death pathways in human osteosarcoma cells
title_sort Decoding the anticancer activity of VO-clioquinol compound: the mechanism of action and cell death pathways in human osteosarcoma cells
dc.creator.none.fl_str_mv León, Ignacio Esteban
Díez, Paula
Baran, Enrique José
Etcheverry, Susana Beatriz
Fuentes, Manuel
author León, Ignacio Esteban
author_facet León, Ignacio Esteban
Díez, Paula
Baran, Enrique José
Etcheverry, Susana Beatriz
Fuentes, Manuel
author_role author
author2 Díez, Paula
Baran, Enrique José
Etcheverry, Susana Beatriz
Fuentes, Manuel
author2_role author
author
author
author
dc.subject.none.fl_str_mv Ciencias Exactas
Química
Ciencias Médicas
vanadium
AKT
cancer
Osteosarcoma
topic Ciencias Exactas
Química
Ciencias Médicas
vanadium
AKT
cancer
Osteosarcoma
dc.description.none.fl_txt_mv Vanadium compounds were studied in recent years by considering them as a representative of a new class of non-platinum metal anticancer drugs. However, a few challenges still remain in the discovery of new molecular targets of these new metallodrugs. Studies on cell signaling pathways related to vanadium compounds have scarcely been reported and so far this information is highly critical for identifying novel targets that play a key role in the antitumor actions of vanadium complexes. This research deals with the alterations in the intracellular signaling pathways promoted by an oxovanadium(IV) complex with the clioquinol (5-chloro-7-iodo-8-quinolinol), VO(CQ)<sub>2</sub>, on a human osteosarcoma cell line (MG-63). Herein are reported, for the first time, the antitumor properties of VO(CQ)<sub>2</sub> and the relative abundance of 224 proteins (which are involved in most of the common intracellular pathways) to identify novel targets of the studied complex. Besides, full-length human recombinant AKT1 kinase was produced by using an IVTT system to evaluate the variation of relative tyrosin-phosphorylation levels caused by this compound. The results of the differential protein expression levels reveal several up-regulated proteins such as CASP3, CASP6, CASP7, CASP10, CASP11, Bcl-x, DAPK and down-regulated ones, such as PKB/AKT, DIABLO, among others. Moreover, cell signaling pathways involved in several altered pathways related to the PKC and AP2 family have been identified in both treatments (2.5 and 10 μM) suggesting the crucial antitumoral role of VO(CQ)<sub>2</sub>. Finally, it has been demonstrated that this compound (10 μM, 6 h) triggers a decrease of 2-fold in <i>in situ</i> AKT1 expression.
Puede accederse a los datos primarios de este trabajo haciendo clic en "Documentos relacionados".
Facultad de Ciencias Exactas
Centro de Química Inorgánica
description Vanadium compounds were studied in recent years by considering them as a representative of a new class of non-platinum metal anticancer drugs. However, a few challenges still remain in the discovery of new molecular targets of these new metallodrugs. Studies on cell signaling pathways related to vanadium compounds have scarcely been reported and so far this information is highly critical for identifying novel targets that play a key role in the antitumor actions of vanadium complexes. This research deals with the alterations in the intracellular signaling pathways promoted by an oxovanadium(IV) complex with the clioquinol (5-chloro-7-iodo-8-quinolinol), VO(CQ)<sub>2</sub>, on a human osteosarcoma cell line (MG-63). Herein are reported, for the first time, the antitumor properties of VO(CQ)<sub>2</sub> and the relative abundance of 224 proteins (which are involved in most of the common intracellular pathways) to identify novel targets of the studied complex. Besides, full-length human recombinant AKT1 kinase was produced by using an IVTT system to evaluate the variation of relative tyrosin-phosphorylation levels caused by this compound. The results of the differential protein expression levels reveal several up-regulated proteins such as CASP3, CASP6, CASP7, CASP10, CASP11, Bcl-x, DAPK and down-regulated ones, such as PKB/AKT, DIABLO, among others. Moreover, cell signaling pathways involved in several altered pathways related to the PKC and AP2 family have been identified in both treatments (2.5 and 10 μM) suggesting the crucial antitumoral role of VO(CQ)<sub>2</sub>. Finally, it has been demonstrated that this compound (10 μM, 6 h) triggers a decrease of 2-fold in <i>in situ</i> AKT1 expression.
publishDate 2017
dc.date.none.fl_str_mv 2017
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
Articulo
http://purl.org/coar/resource_type/c_6501
info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://sedici.unlp.edu.ar/handle/10915/108044
url http://sedici.unlp.edu.ar/handle/10915/108044
dc.language.none.fl_str_mv eng
language eng
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info:eu-repo/semantics/altIdentifier/issn/1756-591X
info:eu-repo/semantics/altIdentifier/doi/10.1039/c7mt00068e
info:eu-repo/semantics/reference/hdl/10915/108112
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
http://creativecommons.org/licenses/by-nc-sa/4.0/
Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0)
eu_rights_str_mv openAccess
rights_invalid_str_mv http://creativecommons.org/licenses/by-nc-sa/4.0/
Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0)
dc.format.none.fl_str_mv application/pdf
891-901
dc.source.none.fl_str_mv reponame:SEDICI (UNLP)
instname:Universidad Nacional de La Plata
instacron:UNLP
reponame_str SEDICI (UNLP)
collection SEDICI (UNLP)
instname_str Universidad Nacional de La Plata
instacron_str UNLP
institution UNLP
repository.name.fl_str_mv SEDICI (UNLP) - Universidad Nacional de La Plata
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