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Title: Integrated molecular signaling involving mitochondrial dysfunction and alteration of cell metabolism induced by tyrosine kinase inhibitors in cancer
Authors: Rodríguez-Hernández, María A.
de la Cruz-Ojeda, P.
López-Grueso, Mª José
Navarro-Villarán, Elena
Requejo-Aguilar, Raquel
Castejón-Vega, Beatriz
Negrete, María
Gallego, Paloma
Vega-Ochoa, Álvaro
Victor, Victor M.
Cordero, Mario D.
Del Campo, José A.
Bárcena, J. Antonio
Padilla, C. Alicia
Muntané, Jordi
metadata.dc.contributor.authoraffiliation: [Rodríguez-Hernández,A; de la Cruz-Ojeda,P; Navarro-Villarán,E; Negrete,M; Vega-Ochoa,A; Muntané,J] Institute of Biomedicine of Seville (IBiS), IBiS/Hospital University “Virgen del Rocío”/CSIC/University of Seville, Seville, Spain. [Rodríguez-Hernández,A; Navarro-Villarán,E; Victor,VM; Muntané,J] Centro de Investigación Biomédica en red de Enfermedades Hepáticas y Digestivas (CIBEREHD), Madrid, Spain. [López-Grueso,MJ; Requejo-Aguilar,R; Bárcena,JA; Padilla,CA] Department of Biochemistry and Molecular Biology, University of Cordoba, Maimonides Biomedical Research Institute of Cordoba (IMIBIC), Cordoba, Spain. [Castejón-Vega,B; Cordero,MD] Research Laboratory, Oral Medicine Department, University of Seville, Seville, Spain. [Gallego,P; Del Campo,JA] Unit for the Clinical Management of Digestive Diseases, Hospital University “Nuestra Señora de Valme”, Sevilla, Spain. [Victor,VM] Service of Endocrinology and Nutrition, Hospital University “Doctor Peset”, Foundation for the Promotion of Health and Biomedical Research in the Valencian Region (FISABIO), Valencia, Spain. [Victor,VM] Department of Physiology, University of Valencia, Valencia, Spain. [Cordero,MD] Department of Physiology, Institute of Nutrition and Food Technology "José Mataix", Biomedical Research Center (CIBM), University of Granada, Armilla, Spain. [Muntané,J] Department of General Surgery, Hospital University “Virgen del Rocío”/IBiS/CSIC/University of Seville, Seville, Spain.
Keywords: Autophagy;Cell death;Endoplasmic reticulum stress;mTOR;Redox status;PGC-1α;Autofagia;Muerte celular;Estrés del retículo endoplásmico;Serina-treonina quinasas TOR;Oxidación-reducción
metadata.dc.subject.mesh: Medical Subject Headings::Phenomena and Processes::Cell Physiological Phenomena::Cell Physiological Processes::Cell Death::Apoptosis
Medical Subject Headings::Phenomena and Processes::Cell Physiological Phenomena::Cell Physiological Processes::Cell Death::Autophagy
Medical Subject Headings::Organisms::Eukaryota::Animals::Chordata::Vertebrates::Mammals::Primates::Haplorhini::Catarrhini::Hominidae::Humans
Medical Subject Headings::Anatomy::Cells::Cellular Structures::Intracellular Space::Cytoplasm::Cytoplasmic Structures::Organelles::Mitochondria
Medical Subject Headings::Chemicals and Drugs::Chemical Actions and Uses::Pharmacologic Actions::Molecular Mechanisms of Pharmacological Action::Enzyme Inhibitors::Protein Kinase Inhibitors
Medical Subject Headings::Chemicals and Drugs::Amino Acids, Peptides, and Proteins::Proteins::Intracellular Signaling Peptides and Proteins::Proto-Oncogene Proteins c-akt
Medical Subject Headings::Phenomena and Processes::Cell Physiological Phenomena::Cellular Microenvironment::Tumor Microenvironment
Medical Subject Headings::Diseases::Neoplasms
Medical Subject Headings::Chemicals and Drugs::Enzymes and Coenzymes::Enzymes::Transferases::Phosphotransferases::Phosphotransferases (Alcohol Group Acceptor)::Phosphatidylinositol 3-Kinases::Phosphatidylinositol 3-Kinase
Issue Date: 2020
Publisher: Elsevier B.V.
Citation: Rodríguez-Hernández MA, de la Cruz-Ojeda P, López-Grueso MJ, Navarro-Villarán E, Requejo-Aguilar R, Castejón-Vega B, et al. Integrated molecular signaling involving mitochondrial dysfunction and alteration of cell metabolism induced by tyrosine kinase inhibitors in cancer. Redox Biol. 2020 Sep;36:101510
Abstract: 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.
metadata.dc.identifier.doi: 10.1016/j.redox.2020.101510
ISSN: 2213-2317
Appears in Collections:01- Artículos - Hospital de Valme
01- Artículos - Hospital Virgen del Rocío
01- Artículos - IBIS. Instituto de Biomedicina de Sevilla
01- Artículos - IMIBIC. Instituto Maimónides de Investigación Biomédica de Córdoba

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