Zhu J, Jiang J, Zhou W, Chen X
Institute of Molecular Medicine and Genetics, Medical College of Georgia, Augusta 30912, USA.
Cancer Res. 1998 Nov 15;58(22):5061-5.
p73, a potential tumor suppressor, is a p53 homologue. Transient over expression of p73 in cells can induce apoptosis and p21, a cellular p53 target gene primarily responsible for p53-dependent cell cycle arrest. To further characterize the role of p73 in tumor suppression, we established several groups of cell lines that inducibly express p73 under a tetracycline-regulated promoter. By using these cell lines, we found that p73 can induce both cell cycle arrest and apoptosis. We also found that p73 can activate some but not all of the previously identified p53 cellular target genes. Furthermore, we found that the transcriptional activities of p53, p73 alpha, and p73 beta to induce their common cellular target genes differ among one another. These results suggest that p73 is both similar to and different from p53 in their signaling pathways leading to tumor suppression.
p73是一种潜在的肿瘤抑制因子，是p53的同源物。在细胞中瞬时过表达p73可诱导细胞凋亡和p21，p21是细胞内p53的靶基因，主要负责p53依赖性细胞周期阻滞。为了进一步阐明p73在肿瘤抑制中的作用，我们建立了几组在四环素调控启动子下可诱导表达p73的细胞系。通过使用这些细胞系，我们发现p73既能诱导细胞周期阻滞，也能诱导细胞凋亡。我们还发现p73能激活一些但不是所有先前确定的p53细胞靶基因。此外，我们发现p53、p73α和p73β诱导其共同细胞靶基因的转录活性彼此不同。这些结果表明，p73在导致肿瘤抑制的信号通路中与p53既有相似之处，也有不同之处。
