Activation of β-catenin by oncogenic PIK3CA and EGFR promotes resistance to glucose deprivation by inducing a strong antioxidant response

Glucose is an essential fuel for cell survival and its availability limits aberrant cellular proliferation. We have hypothesized that specific cancer mutations regulate metabolic response(s) to glucose deprivation (GD). By means of somatic knock-in cellular models, we have analyzed the response to g...

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Veröffentlicht in:	PloS one 2012-05, Vol.7 (5), p.e37526-e37526
Hauptverfasser:	Cardone, Luca, Bardelli, Alberto, Avvedimento, Vittorio Enrico
Format:	Artikel
Sprache:	eng
Schlagworte:	Aberration Activation Adenosine Triphosphate - metabolism Alleles AMP-Activated Protein Kinases - metabolism Antioxidants Antioxidants - metabolism beta Catenin - metabolism Biology Cancer Catalase Cell Death Cell growth Cell Line Cell survival Class I Phosphatidylinositol 3-Kinases Deprivation Epidermal growth factor receptors Epithelial cells Epithelial Cells - metabolism FOXO4 protein Gene expression Glucose Glucose - metabolism Glutathione - metabolism Glycogen Synthase Kinase 3 - metabolism Glycogen Synthase Kinase 3 beta Humans Kinases Mammary gland Mammary Glands, Human - metabolism Medicine Metabolic response Mutation Oxidation-Reduction Oxidative Stress Phosphatidylinositol 3-Kinases - genetics Phosphatidylinositol 3-Kinases - metabolism Receptor, Epidermal Growth Factor - genetics Receptor, Epidermal Growth Factor - metabolism Signaling Superoxide Dismutase - metabolism Synergism Transcription Transcription Factors - metabolism Vascular endothelial growth factor Wnt protein β-Catenin
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