Zhou F, Medh R D, Thompson E B
Department of Human Biological Chemistry and Genetics, The University of Texas Medical Branch, Galveston, TX 77555-0645, USA.
J Steroid Biochem Mol Biol. 2000 Jul-Aug;73(5):195-202. doi: 10.1016/s0960-0760(00)00080-7.
Suppression of c-myc has been implicated as a critical event in some glucocorticoid-evoked apoptotic systems. It is therefore of interest to understand the mechanism of glucocorticoid-regulation of the c-myc gene. In the present study, a detailed analysis of dexamethasone (Dex)-evoked regulation of the human c-myc gene in human leukemic CEM-C7 cells has been performed. Dex suppresses c-myc mRNA and immunoreactive protein expression in clone CEM-C7 and subclone CEM-C7-14 cells. Nuclear run-on assays suggested that the regulation occurred at the level of transcription initiation. The half-life of c-myc mRNA was approximately 30 min and its stability was not affected by Dex treatment. In addition, Dex suppressed luciferase gene expression driven by -2052 to +34 bp c-myc promoter in transfected CEM-C7-14 cells. This result further supports that c-myc gene is suppressed by Dex at the transcriptional level in apoptotic human leukemic cells.
c-myc的抑制被认为是一些糖皮质激素诱发的凋亡系统中的关键事件。因此，了解糖皮质激素对c-myc基因的调控机制很有意义。在本研究中，已对人白血病CEM-C7细胞中地塞米松（Dex）诱发的人c-myc基因调控进行了详细分析。Dex抑制克隆CEM-C7和亚克隆CEM-C7-14细胞中c-myc mRNA和免疫反应性蛋白的表达。核转录分析表明，这种调控发生在转录起始水平。c-myc mRNA的半衰期约为30分钟，其稳定性不受Dex处理的影响。此外，Dex抑制了转染的CEM-C7-14细胞中由-2052至+34 bp的c-myc启动子驱动的荧光素酶基因表达。该结果进一步支持在凋亡的人白血病细胞中，Dex在转录水平抑制c-myc基因。
