Metformin Induces Apoptosis through AMPK-Dependent Inhibition of UPR Signaling in ALL Lymphoblasts

The outcome of patients with resistant phenotypes of acute lymphoblastic leukemia (ALL) or those who relapse remains poor. We investigated the mechanism of cell death induced by metformin in Bp- and T-ALL cell models and primary cells, and show that metformin effectively induces apoptosis in ALL cel...

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Veröffentlicht in:	PloS one Jg. 8; H. 8; S. e74420
Hauptverfasser:	Leclerc, Gilles M., Leclerc, Guy J., Kuznetsov, Jeffim N., DeSalvo, Joanna, Barredo, Julio C.
Format:	Journal Article
Sprache:	Englisch
Veröffentlicht:	United States Public Library of Science 23.08.2013 Public Library of Science (PLoS)
Schlagworte:	Acute lymphoblastic leukemia AKT protein AMP-Activated Protein Kinases - metabolism Analysis Antidiabetics Apoptosis Apoptosis - drug effects Buffers Cancer Cell culture Cell cycle Cell death Cell growth Cell Line Cell Proliferation - drug effects Cell Survival - drug effects Cell Survival - genetics Cytotoxicity Endoplasmic reticulum Endoplasmic Reticulum Stress - drug effects Enzyme inhibitors Gene Expression Regulation, Leukemic - drug effects Hematology Human subjects Humans Inhibitors Kinases Leukemia Lymphatic leukemia Lymphoblasts Lymphocytes T Medical prognosis Medicine Metabolism Metformin Metformin - pharmacology Mortality Oncology Pediatrics Phosphorylation Phosphotransferases Powder injection molding Precursor Cell Lymphoblastic Leukemia-Lymphoma - genetics Precursor Cell Lymphoblastic Leukemia-Lymphoma - metabolism Protein biosynthesis Protein Biosynthesis - drug effects Protein folding Protein synthesis Protein-Serine-Threonine Kinases - genetics Protein-Serine-Threonine Kinases - metabolism Proteins Proto-Oncogene Proteins - genetics Proto-Oncogene Proteins - metabolism Proto-Oncogene Proteins c-akt - genetics Proto-Oncogene Proteins c-akt - metabolism Rapamycin Respiration Restoration Rodents Signal Transduction - drug effects Signaling Stress Stresses Studies Synergism TOR protein TOR Serine-Threonine Kinases - metabolism Toxicity Transcription factors Unfolded Protein Response Florida United States > US
ISSN:	1932-6203, 1932-6203
Online-Zugang:	Volltext
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