Sala A, Casella I, Bellon T, Calabretta B, Watson R J, Peschle C
Thomas Jefferson University, Department of Microbiology and Immunology and Jefferson Cancer Institute, Philadelphia, Pennsylvania 19107, USA.
J Biol Chem. 1996 Apr 19;271(16):9363-7. doi: 10.1074/jbc.271.16.9363.
The retinoblastoma protein family has been implicated in growth control and modulation of the activity of genes involved in cell proliferation, such as B-myb. Recent evidence indicates that the product of the B-myb gene is necessary for the growth and survival of several human and murine cell lines. Upon overexpression, B-myb induces deregulated cell growth of certain cell lines. Here we show that B-myb overexpression is able to induce DNA synthesis in p107 growth-arrested human osteosarcoma cells (SAOS2). p107 might exert its growth-suppressive activity by regulating B-myb gene transcription. Indeed, p107 down-modulated B-myb promoter activity and drastically decreased E2F-mediated transactivation. Finally, B-myb was able to stimulate DNA synthesis of both stably and transiently transfected human glioblastoma cells (T98G). Altogether, these data provide definitive evidence that the human B-myb protein is involved in growth control of human cells, and that p107 has a significant role in regulating B-myb gene activity.
视网膜母细胞瘤蛋白家族与生长控制以及参与细胞增殖的基因（如B-myb）活性的调节有关。最近的证据表明，B-myb基因的产物对于几种人类和鼠类细胞系的生长和存活是必需的。过表达时，B-myb会诱导某些细胞系的细胞生长失控。在此我们表明，B-myb过表达能够在p107生长停滞的人骨肉瘤细胞（SAOS2）中诱导DNA合成。p107可能通过调节B-myb基因转录发挥其生长抑制活性。实际上，p107下调了B-myb启动子活性，并显著降低了E2F介导的反式激活。最后，B-myb能够刺激稳定和瞬时转染的人胶质母细胞瘤细胞（T98G）的DNA合成。总之，这些数据提供了确凿的证据，表明人B-myb蛋白参与人类细胞的生长控制，并且p107在调节B-myb基因活性方面具有重要作用。
