title: The role of heat shock protein 90 in the regulation of tumor cell apoptosis.
abstract: Programmed death of Jurkat tumor cells was studied under conditions of culturing with 17-AAG selective inhibitor of heat shock protein with a molecular weight of 90 kDa and etoposide. Apoptosis realization was evaluated by fluorescent microscopy with FITC-labeled annexin V and propidium iodide. Activity of caspase-3 was evaluated spectrophotometrically. Inhibition of heat shock protein with a molecular weight of 90 kDa activated the apoptotic program in Jurkat tumor cells and etoposide-induced apoptosis. The heat shock protein with a molecular weight of 90 kDa acted as apoptosis inhibitor in tumor cells.
authors.affiliation: Department of Fundamentals of Clinical Medicine, Research and Education Center of Molecular Medicine, Siberian State Medical University, Federal Agency of Health Care and Social Development, Tomsk, Russia. zlobinae@mail.ru
authors.forename: E V
authors.initials: EV
authors.lastname: Kaigorodova
authors.forename: N V
authors.initials: NV
authors.lastname: Ryazantseva
authors.forename: V V
authors.initials: VV
authors.lastname: Novitskii
authors.forename: M V
authors.initials: MV
authors.lastname: Belkina
authors.forename: A N
authors.initials: AN
authors.lastname: Maroshkina
mesh_terms: D017209:Apoptosis / Q000187:drug effects* / Q000502:physiology*; D016227:Benzoquinones / Q000494:pharmacology; D053148:Caspase 3 / Q000096:biosynthesis / Q000378:metabolism; D005047:Etoposide / Q000494:pharmacology; D018841:HSP90 Heat-Shock Proteins / Q000037:antagonists & inhibitors / Q000378:metabolism*; D006801:Humans; D019169:Jurkat Cells; D047029:Lactams, Macrocyclic / Q000494:pharmacology; D009369:Neoplasms / Q000378:metabolism*
chemical_list: D016227:Benzoquinones; D018841:HSP90 Heat-Shock Proteins; D047029:Lactams, Macrocyclic; C112765:tanespimycin; D005047:Etoposide; D053148:Caspase 3