Gope M L, Gope R, Zarucki T
Department of Cell Biology, Baylor College of Medicine, Houston, TX 77030.
Mol Cell Biochem. 1991 May 15;103(2):149-54. doi: 10.1007/BF00227481.
Human A431 carcinoma cell line is known to have 30 fold amplified epidermal growth factor receptor (EGF-R) gene. We have studied the effect of steroid hormone dexamethasone (DEX) and protein synthesis inhibitor cycloheximide (CHX) on the expression of EGF-R gene in this cell line. DEX treatment and protein synthesis inhibition by CHX treatment cause a rapid 3 to 4 fold increase in the level of EGF-R mRNA and combined treatment of the above two agents have less than additive effect. It appears that mRNA for EGF-R accumulate within the cell during protein synthesis inhibition and upon removal of CHX, gets translated into EGF-R specific protein as judged by immuno-dot assay. We did not observe the phenomenon of 'super induction' nor much of an additive effect under condition of combined DEX and CHX treatment.
已知人类A431癌细胞系具有30倍扩增的表皮生长因子受体（EGF-R）基因。我们研究了类固醇激素地塞米松（DEX）和蛋白质合成抑制剂环己酰亚胺（CHX）对该细胞系中EGF-R基因表达的影响。DEX处理以及CHX处理导致的蛋白质合成抑制会使EGF-R mRNA水平迅速升高3至4倍，而上述两种试剂的联合处理效果小于相加效应。似乎在蛋白质合成抑制期间，EGF-R的mRNA在细胞内积累，并且在去除CHX后，通过免疫斑点测定判断，其会被翻译成EGF-R特异性蛋白。在DEX和CHX联合处理的条件下，我们未观察到“超诱导”现象，也未观察到明显的相加效应。
