Integrated molecular signaling involving mitochondrial dysfunction and alteration of cell metabolism induced by tyrosine kinase inhibitors in cancer

Cancer cells have unlimited replicative potential, insensitivity to growth-inhibitory signals, evasion of apoptosis, cellular stress, and sustained angiogenesis, invasiveness and metastatic potential. Cancer cells adequately adapt cell metabolism and integrate several intracellular and redox signali...

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Autores: Rodríguez-Hernández, María A., Cruz, Patricia de la, López-Grueso, M. José, Navarro-Villarán, Elena, Requejo-Aguilar, Raquel, Castejón Vega, Beatriz, Negrete, María, Gallego, Paloma, Vega-Ochoa, Álvaro, Victor, Víctor M., Cordero, Mario D., Campo, José A. del, Bárcena, José Antonio, Padilla, Alicia C., Muntané, Jordi
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:2020
País:España
Institución:Consejo Superior de Investigaciones Científicas (CSIC)
Repositorio:DIGITAL.CSIC. Repositorio Institucional del CSIC
OAI Identifier:oai:digital.csic.es:10261/230871
Acceso en línea:http://hdl.handle.net/10261/230871
Access Level:acceso abierto
Palabra clave:Autophagy
Cell death
Endoplasmic reticulum stress
mTOR
Redox status
PGC-1α
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oai_identifier_str oai:digital.csic.es:10261/230871
network_acronym_str ES
network_name_str España
repository_id_str
dc.title.none.fl_str_mv Integrated molecular signaling involving mitochondrial dysfunction and alteration of cell metabolism induced by tyrosine kinase inhibitors in cancer
title Integrated molecular signaling involving mitochondrial dysfunction and alteration of cell metabolism induced by tyrosine kinase inhibitors in cancer
spellingShingle Integrated molecular signaling involving mitochondrial dysfunction and alteration of cell metabolism induced by tyrosine kinase inhibitors in cancer
Rodríguez-Hernández, María A.
Autophagy
Cell death
Endoplasmic reticulum stress
mTOR
Redox status
PGC-1α
title_short Integrated molecular signaling involving mitochondrial dysfunction and alteration of cell metabolism induced by tyrosine kinase inhibitors in cancer
title_full Integrated molecular signaling involving mitochondrial dysfunction and alteration of cell metabolism induced by tyrosine kinase inhibitors in cancer
title_fullStr Integrated molecular signaling involving mitochondrial dysfunction and alteration of cell metabolism induced by tyrosine kinase inhibitors in cancer
title_full_unstemmed Integrated molecular signaling involving mitochondrial dysfunction and alteration of cell metabolism induced by tyrosine kinase inhibitors in cancer
title_sort Integrated molecular signaling involving mitochondrial dysfunction and alteration of cell metabolism induced by tyrosine kinase inhibitors in cancer
dc.creator.none.fl_str_mv Rodríguez-Hernández, María A.
Cruz, Patricia de la
López-Grueso, M. José
Navarro-Villarán, Elena
Requejo-Aguilar, Raquel
Castejón Vega, Beatriz
Negrete, María
Gallego, Paloma
Vega-Ochoa, Álvaro
Victor, Víctor M.
Cordero, Mario D.
Campo, José A. del
Bárcena, José Antonio
Padilla, Alicia C.
Muntané, Jordi
author Rodríguez-Hernández, María A.
author_facet Rodríguez-Hernández, María A.
Cruz, Patricia de la
López-Grueso, M. José
Navarro-Villarán, Elena
Requejo-Aguilar, Raquel
Castejón Vega, Beatriz
Negrete, María
Gallego, Paloma
Vega-Ochoa, Álvaro
Victor, Víctor M.
Cordero, Mario D.
Campo, José A. del
Bárcena, José Antonio
Padilla, Alicia C.
Muntané, Jordi
author_role author
author2 Cruz, Patricia de la
López-Grueso, M. José
Navarro-Villarán, Elena
Requejo-Aguilar, Raquel
Castejón Vega, Beatriz
Negrete, María
Gallego, Paloma
Vega-Ochoa, Álvaro
Victor, Víctor M.
Cordero, Mario D.
Campo, José A. del
Bárcena, José Antonio
Padilla, Alicia C.
Muntané, Jordi
author2_role author
author
author
author
author
author
author
author
author
author
author
author
author
author
dc.contributor.none.fl_str_mv Instituto de Salud Carlos III
Junta de Andalucía
Generalitat Valenciana
Red Temática de Investigación Cooperativa en Enfermedades Cardiovasculares (España)
Centro de Investigación Biomédica en Red Enfermedades Hepáticas y Digestivas (España)
European Commission
Ministerio de Economía y Competitividad (España)
Consejo Superior de Investigaciones Científicas [https://ror.org/02gfc7t72]
dc.subject.none.fl_str_mv Autophagy
Cell death
Endoplasmic reticulum stress
mTOR
Redox status
PGC-1α
topic Autophagy
Cell death
Endoplasmic reticulum stress
mTOR
Redox status
PGC-1α
description Cancer cells have unlimited replicative potential, insensitivity to growth-inhibitory signals, evasion of apoptosis, cellular stress, and sustained angiogenesis, invasiveness and metastatic potential. Cancer cells adequately adapt cell metabolism and integrate several intracellular and redox signaling to promote cell survival in an inflammatory and hypoxic microenvironment in order to maintain/expand tumor phenotype. The administration of tyrosine kinase inhibitor (TKI) constitutes the recommended therapeutic strategy in different malignancies at advanced stages. There are important interrelationships between cell stress, redox status, mitochondrial function, metabolism and cellular signaling pathways leading to cell survival/death. The induction of apoptosis and cell cycle arrest widely related to the antitumoral properties of TKIs result from tightly controlled events involving different cellular compartments and signaling pathways. The aim of the present review is to update the most relevant studies dealing with the impact of TKI treatment on cell function. The induction of endoplasmic reticulum (ER) stress and Ca2+ disturbances, leading to alteration of mitochondrial function, redox status and phosphatidylinositol 3-kinase (PI3K)-protein kinase B (Akt)-mammalian target of rapamycin (mTOR) and AMP-activated protein kinase (AMPK) signaling pathways that involve cell metabolism reprogramming in cancer cells will be covered. Emphasis will be given to studies that identify key components of the integrated molecular pattern including receptor tyrosine kinase (RTK) downstream signaling, cell death and mitochondria-related events that appear to be involved in the resistance of cancer cells to TKI treatments.
publishDate 2020
dc.date.none.fl_str_mv 2020
2021
2021
2021
dc.type.none.fl_str_mv info:eu-repo/semantics/article
http://purl.org/coar/resource_type/c_dcae04bc
Publisher's version
info:eu-repo/semantics/publishedVersion
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/10261/230871
url http://hdl.handle.net/10261/230871
dc.language.none.fl_str_mv Inglés
language_invalid_str_mv Inglés
dc.relation.none.fl_str_mv #PLACEHOLDER_PARENT_METADATA_VALUE#
info:eu-repo/grantAgreement/MINECO/Plan Estatal de Investigación Científica y Técnica y de Innovación 2013-2016/BFU2016-80006-P
http://doi.org/10.1016/j.redox.2020.101510
Sí
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
dc.publisher.none.fl_str_mv Elsevier
publisher.none.fl_str_mv Elsevier
dc.source.none.fl_str_mv reponame:DIGITAL.CSIC. Repositorio Institucional del CSIC
instname:Consejo Superior de Investigaciones Científicas (CSIC)
instname_str Consejo Superior de Investigaciones Científicas (CSIC)
reponame_str DIGITAL.CSIC. Repositorio Institucional del CSIC
collection DIGITAL.CSIC. Repositorio Institucional del CSIC
repository.name.fl_str_mv
repository.mail.fl_str_mv
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spelling Integrated molecular signaling involving mitochondrial dysfunction and alteration of cell metabolism induced by tyrosine kinase inhibitors in cancerRodríguez-Hernández, María A.Cruz, Patricia de laLópez-Grueso, M. JoséNavarro-Villarán, ElenaRequejo-Aguilar, RaquelCastejón Vega, BeatrizNegrete, MaríaGallego, PalomaVega-Ochoa, ÁlvaroVictor, Víctor M.Cordero, Mario D.Campo, José A. delBárcena, José AntonioPadilla, Alicia C.Muntané, JordiAutophagyCell deathEndoplasmic reticulum stressmTORRedox statusPGC-1αCancer cells have unlimited replicative potential, insensitivity to growth-inhibitory signals, evasion of apoptosis, cellular stress, and sustained angiogenesis, invasiveness and metastatic potential. Cancer cells adequately adapt cell metabolism and integrate several intracellular and redox signaling to promote cell survival in an inflammatory and hypoxic microenvironment in order to maintain/expand tumor phenotype. The administration of tyrosine kinase inhibitor (TKI) constitutes the recommended therapeutic strategy in different malignancies at advanced stages. There are important interrelationships between cell stress, redox status, mitochondrial function, metabolism and cellular signaling pathways leading to cell survival/death. The induction of apoptosis and cell cycle arrest widely related to the antitumoral properties of TKIs result from tightly controlled events involving different cellular compartments and signaling pathways. The aim of the present review is to update the most relevant studies dealing with the impact of TKI treatment on cell function. The induction of endoplasmic reticulum (ER) stress and Ca2+ disturbances, leading to alteration of mitochondrial function, redox status and phosphatidylinositol 3-kinase (PI3K)-protein kinase B (Akt)-mammalian target of rapamycin (mTOR) and AMP-activated protein kinase (AMPK) signaling pathways that involve cell metabolism reprogramming in cancer cells will be covered. Emphasis will be given to studies that identify key components of the integrated molecular pattern including receptor tyrosine kinase (RTK) downstream signaling, cell death and mitochondria-related events that appear to be involved in the resistance of cancer cells to TKI treatments.This study was funded by Institute of Health Carlos III (ISCiii) (PI16/00090, PI19/00838 and PI19/01266), Spanish Ministry of Economy and Competitiveness (BFU2016-80006-P), Andalusian Ministry of Economy, Innovation, Science and Employment (BIO-216 and CTS-6264), Andalusian Ministry of Equality, Health and Social Policies (PI-0198-2016) and Valencian Ministry of Education, Culture and Sports (PROMETEO/2019/027). P de la C-O was supported by FPU predoctoral fellowship (FPU17/00026) from Spanish Ministry of Education, Culture and Sports. E N-V was supported by the the predoctoral i-PFIS IIS-enterprise contract in science and technologies in health (IFI18/00014) from ISCiii. We thank the Biomedical Research Network Center for Cardiovascular Diseases (CIBERcv), and the Biomedical Research Network Center for Liver and Digestive Diseases (CIBERehd) founded by the ISCiii and co-financed by European Regional Development Fund (ERDF) "A way to achieve Europe" for their financial support.ElsevierInstituto de Salud Carlos IIIJunta de AndalucíaGeneralitat ValencianaRed Temática de Investigación Cooperativa en Enfermedades Cardiovasculares (España)Centro de Investigación Biomédica en Red Enfermedades Hepáticas y Digestivas (España)European CommissionMinisterio de Economía y Competitividad (España)Consejo Superior de Investigaciones Científicas [https://ror.org/02gfc7t72]2021202120202021info:eu-repo/semantics/articlehttp://purl.org/coar/resource_type/c_dcae04bcPublisher's versioninfo:eu-repo/semantics/publishedVersionhttp://hdl.handle.net/10261/230871reponame:DIGITAL.CSIC. Repositorio Institucional del CSICinstname:Consejo Superior de Investigaciones Científicas (CSIC)Inglés#PLACEHOLDER_PARENT_METADATA_VALUE#info:eu-repo/grantAgreement/MINECO/Plan Estatal de Investigación Científica y Técnica y de Innovación 2013-2016/BFU2016-80006-Phttp://doi.org/10.1016/j.redox.2020.101510Síinfo:eu-repo/semantics/openAccessoai:digital.csic.es:10261/2308712026-05-22T06:33:51Z
score 15,811543

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