RT Journal Article
T1 Integrated molecular signaling involving mitochondrial dysfunction and alteration of cell metabolism induced by tyrosine kinase inhibitors in cancer
A1 Rodríguez-Hernández, María A.
A1 de la Cruz-Ojeda, P.
A1 López-Grueso, Mª José
A1 Navarro-Villarán, Elena
A1 Requejo-Aguilar, Raquel
A1 Castejón-Vega, Beatriz
A1 Negrete, María
A1 Gallego, Paloma
A1 Vega-Ochoa, Álvaro
A1 Victor, Victor M.
A1 Cordero, Mario D.
A1 Del Campo, José A.
A1 Bárcena, J. Antonio
A1 Padilla, C. Alicia
A1 Muntané, Jordi
K1 Autophagy
K1 Cell death
K1 Endoplasmic reticulum stress
K1 mTOR
K1 Redox status
K1 PGC-1α
K1 Autofagia
K1 Muerte celular
K1 Estrés del retículo endoplásmico
K1 Serina-treonina quinasas TOR
K1 Oxidación-reducción
AB 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.
PB Elsevier B.V.
YR 2020
FD 2020
LK http://hdl.handle.net/10668/3608
UL http://hdl.handle.net/10668/3608
LA en
NO 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
DS RISalud
RD Apr 7, 2025