Cell fate decision mechanism by the transcription factor E2F in cell growth and tumor suppression

我们分析了由转录因子E2F介导的控制细胞生长和肿瘤抑制的分子机制，E2F是肿瘤抑制因子pRB的主要靶点。我们确定了5个新的基因，这是特异性激活的E2F诱导的pRB功能的丧失，一个代表性的致癌变化。这些基因产物中的许多参与诱导细胞死亡的p53途径。PI3激酶通路不能抑制pRB功能丧失引起的E2F对抑癌基因的激活。

We analyzed the molecular mechanism of control of cell growth and tumor suppression mediated by the transcription factor E2F, the main target of the tumor suppressor pRB. We identified 5 novel genes, which are specifically activated by E2F induced by loss of pRB function, a representative oncogenic change. Many of these gene products are involved in the p53 pathway, which induces cell death. PI3 kinase pathway did not suppress activation of tumor suppressor genes by E2F induced by loss of pRB function.