Kelly K, Cochran B H, Stiles C D, Leder P
Cell. 1983 Dec;35(3 Pt 2):603-10. doi: 10.1016/0092-8674(83)90092-2.
We show that c-myc is an inducible gene that is regulated by specific growth signals in a cell-cycle-dependent manner. Specifically, agents that initiate the first phase of a proliferative response in lymphocytes (lipopolysaccharide or Concanavalin A) and fibroblasts (platelet-derived growth factor) induce c-myc mRNA. Within one to three hr after the addition of these mitogens to the appropriate cells, c-myc mRNA concentration is increased between 10- and 40-fold. This induction of c-myc mRNA occurs in the presence of cycloheximide and, therefore, does not require the synthesis of new protein species. Consequently, the induction of c-myc mRNA is not secondary to growth. In addition, c-myc mRNA is "superinduced" by the combination of cycloheximide and mitogen, a finding consistent with a model that a labile protein may regulate c-myc levels in these cells. Further, this work suggests a regulatory linkage between the function of two oncogenes--c-myc and c-sis--the latter being the putative structural gene for PDGF.
我们发现c-myc是一个可诱导基因，它受特定生长信号的调控，且这种调控依赖于细胞周期。具体而言，能引发淋巴细胞（脂多糖或伴刀豆球蛋白A）和成纤维细胞（血小板衍生生长因子）增殖反应第一阶段的因子可诱导c-myc mRNA的产生。在向相应细胞添加这些促有丝分裂原后的1至3小时内，c-myc mRNA浓度增加了10至40倍。c-myc mRNA的这种诱导在放线菌酮存在的情况下也会发生，因此，它不需要合成新的蛋白质种类。所以，c-myc mRNA的诱导并非生长的继发结果。此外，放线菌酮和促有丝分裂原的联合作用会使c-myc mRNA“超诱导”，这一发现与一种模型相符，即一种不稳定的蛋白质可能调节这些细胞中c-myc的水平。此外，这项研究表明了两个癌基因——c-myc和c-sis——功能之间的调控联系，后者是PDGF的假定结构基因。
