Действие ингибиторов белков теплового шока 90 и 27 на дексаметазониндуцированный апоптоз опухолевых клеток

Programmed cell death of tumor cells of line Jurkat in conditions of cultivation with various concentration of dexamethasone, selective inhibitors of Hsp90 (Heat shock protein — Hsp) (17-AAG) and Hsp27 (KRIBB3) was investigated. An estimation of realisation apoptosis spent by method of fluorescent microscopy with use annexin V-FITC and propidium iodide. Inhibition of Hsp90 and Hsp27 leads to activation of tumor cells Jurkat apoptotic program and strengthening of dexamethasone-induced apoptosis. Hsp27 and Hsр90 play an antiapoptotic role in tumor cells of line Jurkat.Представлено исследование программированной гибели опухолевых клеток линии Jurkat в условиях культивирования с различными концентрациями дексаметазона, селективными ингибиторами Hsp90 (Heat shock protein — Hsp) (17-AAG) и Hsp27 (KRIBB3). Оценку реализации апоптоза проводили методом флюоресцентной микроскопии с использованием FITCмеченного аннексина V и пропидий йодида. Ингибирование Hsp90 и Hsp27 приводит к активации апоптотической программы опухолевых клеток Jurkat и усилению дексаметазониндуцированного апоптоза. В опухолевых клетках Hsp27 и Hsр90 играют роль ингибиторов апоптоза

Action of inhibitors Heat shock proteins 90 and 27 on dexamethasone-induced apoptosis of tumor cells

Programmed cell death of tumor cells of line Jurkat in conditions of cultivation with various concentration of dexamethasone, selective inhibitors of Hsp90 (Heat shock protein — Hsp) (17-AAG) and Hsp27 (KRIBB3) was investigated. An estimation of realisation apoptosis spent by method of fluorescent microscopy with use annexin V-FITC and propidium iodide. Inhibition of Hsp90 and Hsp27 leads to activation of tumor cells Jurkat apoptotic program and strengthening of dexamethasone-induced apoptosis. Hsp27 and Hsр90 play an antiapoptotic role in tumor cells of line Jurkat

RECEPTOR SUPERFAMILY OF TUMOR NECROSIS FACTOR Α, AND HSP90 HEAT SHOCK PROTEIN: A MOLECULAR BASIS FOR INTERACTIONS

Abstract.  A  study  was  performed  aiming  to  investigate  interactions  between  TNFα  receptor  (TNF1) superfamily and heat shock protein Hsp90, using a Jurkat tumor cell line. The tumor cells cultured in presence of Hsp90 inhibitor (17-AAG) showed increased numbers of cells, presenting surface TNFR1 and FasR, which facilitate  triggering  of  programmed  cell  death.  It  was  also  revealed  that  Hsp90  blockage  under  the  in  vitro conditions causes a decrease in FasL, while not affecting TNFα and sTNFR1 production by the tumor cells. (Med. Immunol., 2011, vol. 13, N 2-3, pp 247-252