Tumor-associated mutant p53 promotes cancer cell survival upon glutamine deprivation through p21 induction

Cancer cells depend on glutamine to sustain their increased proliferation and manage oxidative stress, yet glutamine is often depleted at tumor sites owing to excessive cellular consumption and poor vascularization. We have previously reported that p53 protein, although a well-known tumor suppressor...

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Veröffentlicht in:	Oncogene 2017-04, Vol.36 (14), p.1991-2001
Hauptverfasser:	Tran, T Q, Lowman, X H, Reid, M A, Mendez-Dorantes, C, Pan, M, Yang, Y, Kong, M
Format:	Artikel
Sprache:	eng
Schlagworte:	38/89 631/67/2327 631/80/86 64/60 82/1 96/106 96/109 96/2 96/95 Amino acids Animals Apoptosis Cancer Carcinogenesis Cell Biology Cell cycle Cell growth Cell proliferation Cell survival Cell Survival - drug effects Cell Survival - genetics Cells, Cultured Cyclin-Dependent Kinase Inhibitor p21 - genetics Cyclin-Dependent Kinase Inhibitor p21 - metabolism Gene expression Gene Expression Regulation, Neoplastic Genetic aspects Glutamine Glutamine - deficiency Glutamine - metabolism HCT116 Cells Health aspects Human Genetics Humans Internal Medicine Lymphoma Medicine Medicine & Public Health Metabolism Mice Mice, Nude Mutant Proteins - genetics Mutant Proteins - metabolism Mutants Mutation Neoplasms - genetics Neoplasms - metabolism Neoplasms - pathology Null cells Oncology original-article Oxidative stress p53 Protein Stress, Physiological - genetics Tumor proteins Tumor suppressor genes Tumor Suppressor Protein p53 - genetics Tumor Suppressor Protein p53 - metabolism Tumors Up-Regulation - genetics Vascularization
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