The potential tumor suppressor p73 differentially regulates cellular p53 target genes.
The potential tumor suppressor p73 differentially regulates cellular p53 target genes.
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发表时间：
1998-11
期刊：
影响因子：
11.2
通讯作者：
Jian‐hui Zhu;Jieyuan Jiang;Wenjing Zhou;Xinbin Chen
中科院分区：
文献类型：
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作者：
Jian‐hui Zhu;Jieyuan Jiang;Wenjing Zhou;Xinbin Chen
p73是一种潜在的肿瘤抑制因子，是p53的同源物。p73在细胞中的瞬时过表达可以诱导细胞凋亡和p21，一种主要负责p53依赖性细胞周期阻滞的细胞p53靶基因。为了进一步表征p73在肿瘤抑制中的作用，我们建立了几组在四环素调节的启动子下诱导表达p73的细胞系。通过使用这些细胞系，我们发现p73可以诱导细胞周期阻滞和凋亡。我们还发现，p73可以激活一些，但不是所有的先前确定的p53细胞靶基因。此外，我们发现p53、p73 α和p73 β诱导其共同的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既相似又不同。
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.