DIM-C-pPhCO2Me

DIM-C-pPhCO2Me抑制了ACHN和786-O细胞的生长并诱导了凋亡[1]。DIM-C-pPhCO2Me降低了RMS细胞中NR4A1依赖的转激活作用，并抑制了RMS细胞和肿瘤的生长，诱导了凋亡。NR4A1的敲除和DIM-C-pPhCO2Me的处理均诱导了ROS产生，这激活了应激基因并诱导了sestrin 2的产生，后者激活了AMPK并抑制了突变型p53 RMS细胞中的mTOR[2]。

DMSO:50 mg/mL (131.43 mM)

Knockdown of NR4A1 in ACHN and 786-O cells was carried out using Lipofectamine 2000 reagent according to the manufacturer's protocol. siRNA complexes used in the study are as follows: siGL2-5', CGU ACG CGG AAU ACU UCG A; siNR4A1 (1)-SASI_Hs02_00333289; siNR4A1 (2)-SASI_Hs01_00182072. ACHN RCC cells were plated on 12-well plates at 5 x 104 cells per well in DMEM supplemented with 2.5% charcoal-stripped FBS. After 24 hr, various amounts of DNA [NBRE3-luc (400 ng), FLAG-NR4A1 (40 ng)] were cotransfected into each well by Lipofectamine 2000 reagent according to the manufacturer's protocol. After 6 hr of transfection, cells were treated with 2.5% stripped DMEM containing either DMSO, DIM-C-pPhOH (20 μM) or DIM-C-pPhCO2Me (15 μM) for 18 hr [1].