KRIBB11

HSF1:1.2 μM

在小鼠异种移植模型中，与未经处理的对照小鼠相比，KRIBB11治疗可使肿瘤体积减少47%。此外，接受KRIBB11处理的小鼠肿瘤中HSP70蛋白水平显著降低，这支持了KRIBB11通过抑制HSF1发挥其体内抗肿瘤活性的观点[1]。

KRIBB11以浓度依赖的方式抑制HSF1活性。它降调HSP70和HSP27的表达。KRIBB11能够抑制癌症细胞增殖，使细胞周期在G2/M阶段停滞并诱导凋亡。但它不抑制热激诱导的HSF1向hsp70启动子的招募或HSF1 Ser-230的磷酸化。KRIBB11抑制热激诱导的pTEFb向hsp70启动子的招募以及p-TEFb依赖的polⅡ CTD Ser-2的磷酸化[1]。

H2O:< 1 mg/mL (insoluble or slightly soluble);DMSO:3 mg/mL (10.55 mM);Ethanol:< 1 mg/mL (insoluble or slightly soluble)

HCT-116 cells are treated with KRIBB11 at various concentrations for 48 h. Cells are then harvested by trypsinization, fixed with 70% chilled ethanol, and preserved at ?20 °C before FACS analysis. Fixed cells are washed twice with phosphate-buffered saline (PBS) solution before being suspended in 500 μl of PBS and treated with 100 mg/ml RNase A at 37 °C for 30 min. Propidium iodide is then added to a final concentration of 50 mg/ml for DNA staining, and 20,000 fixed cells are analyzed on a FACSCalibur system. Cell cycle distribution is analyzed using the ModFit program.(Only for Reference)