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Título

Oncogenic p95HER2/611CTF primes human breast epithelial cells for metabolic stress-induced down-regulation of FLIP and activation of TRAIL-R/Caspase-8-dependent apoptosis

AutorMartín-Pérez, Rosa CSIC; Yerbes, Rosario CSIC ORCID; Mora-Molina, Rocío CSIC ORCID; Cano-González, Ana CSIC; Arribas, Joaquín; Mazzone, Massimiliano; López-Rivas, Abelardo CSIC ORCID; Palacios, Carmen CSIC ORCID
Palabras clavemTOR
FLIP
Metabolic stress
TRAIL-R
p95HER2/611CTF
Fecha de publicación2017
EditorImpact Journals
CitaciónOncotarget 8(55): 93688-93703 (2017)
ResumenOncogenic transformation triggers reprogramming of cell metabolism, as part of the tumorigenic process. However, metabolic reprogramming may also increase the sensitivity of transformed cells to microenvironmental stress, at the early stages of tumor development. Herein, we show that transformation of human breast epithelial cells by the p95HER2/611CTF oncogene markedly sensitizes these cells to metabolic stress induced by the simultaneous inhibition of glucose and glutamine metabolism. In p95HER2/611CTF-transformed cells, metabolic stress activates a TNF related apoptosis-inducing ligand (TRAIL)-R and caspase-8-dependent apoptotic process that requires prior down-regulation of cellular FLICE-like inhibitor protein (c-FLIP) levels. Importantly, sustained mTOR activation is involved in FLIP down-regulation and apoptosis induced by metabolic stress. In vivo experiments in immunodeficient mice demonstrate a requirement for caspase-8 in restraining primary tumor growth of xenografts with p95HER2/611CTF-transformed cells. Collectively, these data define a critical role of the extrinsic pathway of apoptosis in the control of tumor initiation by microenvironmental cues.
Versión del editorhttps://doi.org/10.18632/oncotarget.21458
URIhttp://hdl.handle.net/10261/165662
DOI10.18632/oncotarget.21458
Identificadoresdoi: 10.18632/oncotarget.21458
e-issn: 1949-2553
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