Oncogenic transformation potentiates apoptosis, S-phase arrest and stress-kinase activation by etoposide

The exact mechanisms for the selective toxicity of chemotherapeutic drugs against tumor cells are not fully understood. We designed a series of experiments to test the possibility that the positive proliferative signal initiated by oncogenes might change the sensitivity for apoptosis induction by th...

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Veröffentlicht in:	Oncogene 1997-10, Vol.15 (14), p.1643-1651
Hauptverfasser:	CHEN, G, SHU, J, STACEY, D. W
Format:	Artikel
Sprache:	eng
Schlagworte:	3T3 Cells Animals Antitumor agents Apoptosis Apoptosis - drug effects Biological and medical sciences Calcium-Calmodulin-Dependent Protein Kinases - metabolism Cell activation Cell cycle Cell physiology Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes Cell Transformation, Neoplastic - drug effects Cyclin-dependent kinase Cyclin-Dependent Kinase Inhibitor p21 Cyclin-dependent kinases Cyclins - metabolism DNA Fragmentation DNA topoisomerase (ATP-hydrolysing) Enzyme Activation - drug effects Enzyme inhibitors Enzyme Inhibitors - pharmacology Etoposide Etoposide - pharmacology Extracellular signal-regulated kinase Fundamental and applied biological sciences. Psychology Genetic transformation JNK Mitogen-Activated Protein Kinases Kinases MAP kinase Mice Mitogen-Activated Protein Kinase 3 Mitogen-Activated Protein Kinases Molecular and cellular biology p53 Protein Raf protein S Phase Topoisomerase II Inhibitors Toxicity Transformed cells Tumor cells VP16 protein
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