Synthetic lethality of combined glutaminase and Hsp90 inhibition in mTORC1-driven tumor cells

Significance The mammalian target of rapamycin complex 1 (mTORC1)-mediated signaling regulates protein translation, cell size/growth, cell survival, and metabolism. This signaling is commonly deregulated in cancer as well as genetic disorders such as tuberous sclerosis complex and sporadic lymphangi...

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Veröffentlicht in:	Proceedings of the National Academy of Sciences - PNAS 2015-01, Vol.112 (1), p.E21-E29
Hauptverfasser:	Li, Jing, Csibi, Alfredo, Yang, Sun, Hoffman, Gregory R., Li, Chenggang, Zhang, Erik, Yu, Jane J., Blenis, John
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals Apoptosis - drug effects Benzoquinones - pharmacology Biological Sciences Biosynthesis cell death Cell Line, Tumor Cell Shape - drug effects Cell Survival - drug effects cell viability Endoplasmic reticulum genetic disorders Glutamate Dehydrogenase - antagonists & inhibitors Glutamate Dehydrogenase - metabolism glutaminase Glutaminase - antagonists & inhibitors Glutaminase - metabolism Glutamine - metabolism Heat shock proteins HSP90 Heat-Shock Proteins - antagonists & inhibitors HSP90 Heat-Shock Proteins - metabolism Humans Lactams, Macrocyclic - pharmacology mammals Mechanistic Target of Rapamycin Complex 1 metabolism Mice Models, Biological Multiprotein Complexes - metabolism neoplasm cells neoplasms Oxidation-Reduction - drug effects Oxidative stress Phenotype PNAS Plus Proteins sclerosis Signal transduction Sirolimus - pharmacology Small Molecule Libraries - pharmacology Sulfides - pharmacology Thiadiazoles - pharmacology TOR Serine-Threonine Kinases - metabolism Tuberous Sclerosis - metabolism Tuberous Sclerosis - pathology Tuberous Sclerosis Complex 2 Protein Tumor Suppressor Proteins - deficiency Tumor Suppressor Proteins - metabolism Tumors Xenograft Model Antitumor Assays
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