Chang J D, Kennedy A R
Department of Cancer Biology, Harvard University School of Public Health, Boston, MA 02115.
Carcinogenesis. 1988 Jan;9(1):17-20. doi: 10.1093/carcin/9.1.17.
Normally, when confluent cells are stimulated to divide, they show a transient increase in c-myc RNA levels (1-5). This has led many investigators to believe that the rise in c-myc RNA is causally related to the control and regulation of cell proliferation. However, we report here that the rise in c-myc RNA levels is not observed in stimulated cycling C3H 10T1/2 and 3T3 cells that have been grown to confluence in the presence of the protease inhibitor antipain. Cells continue to progress from the G0/G1 phase to S phase of the cell cycle in the absence of an increase in c-myc RNA; the kinetics of [3H]thymidine incorporation after serum stimulation are comparable to those observed in cells in which c-myc RNA levels rise after serum stimulation. Our observations are of significance because they suggest a dissociation between the transient rise of c-myc RNA which occurs before DNA synthesis and the events that initiate DNA synthesis in quiescent fibroblasts; c-myc may not play as central a role in stimulating noncycling, quiescent cells to progress through the cell cycle, as has been generally assumed.
正常情况下,当汇合的细胞受到刺激开始分裂时,它们的c-myc RNA水平会出现短暂升高(1 - 5)。这使得许多研究人员认为,c-myc RNA的升高与细胞增殖的控制和调节存在因果关系。然而,我们在此报告,在含有蛋白酶抑制剂抗痛素的情况下生长至汇合状态的受刺激循环C3H 10T1/2和3T3细胞中,未观察到c-myc RNA水平的升高。在没有c-myc RNA增加的情况下,细胞继续从细胞周期的G0/G1期进入S期;血清刺激后[3H]胸苷掺入的动力学与在血清刺激后c-myc RNA水平升高的细胞中观察到的动力学相当。我们的观察结果具有重要意义,因为它们表明在DNA合成之前发生的c-myc RNA的短暂升高与静止成纤维细胞中启动DNA合成的事件之间存在脱节;c-myc在刺激非循环静止细胞通过细胞周期方面可能不像通常所认为的那样发挥核心作用。