p63 heterozygous mutant mice are not prone to spontaneous or chemically induced tumors
p63 heterozygous mutant mice are not prone to spontaneous or chemically induced tumors
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DOI：
10.1073/pnas.0602477103
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发表时间：
2006-05-30
影响因子：
11.1
通讯作者：
Mills, Alea A.
中科院分区：
文献类型：
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作者：
Keyes, William M.;Vogel, Hannes;Mills, Alea A.
P63和p53之间的同源性表明，这些蛋白的功能可能相似。然而，来自人类肿瘤的大多数数据并没有支持p63在肿瘤抑制中的类似作用。为了研究这个问题，我们研究了在WT和p53受损背景下p63+/-小鼠的自发肿瘤发生。我们发现p63+/-小鼠不容易患肿瘤，p63和p53杂合子小鼠的肿瘤比p53+/-小鼠少。在p63基因受损的小鼠身上出现的罕见肿瘤也与P53+/-小鼠的肿瘤不同。此外，p63+/-小鼠不容易发生化学诱导的肿瘤形成，p63在肿瘤中的表达保持不变。这些发现表明，与来自人类肿瘤的数据一致，p63在癌症中发挥的生物学作用与p53明显不同。
Homology between p63 and p53 has suggested that these proteins might function similarly. However, the majority of data from human tumors have not supported a similar role for p63 in tumor suppression. To investigate this issue, we studied spontaneous tumorigenesis in p63+/- mice in both WT and p53-compromised backgrounds. We found that p63+/- mice were not tumor prone and mice heterozygous for both p63 and p53 had fewer tumors than p53+/- mice. The rare tumors that developed in mice with compromised p63 were also distinct from those of p53+/- mice. Furthermore, p63+/- mice were not prone to chemically induced tumorigenesis, and p63 expression was maintained in carcinomas. These findings demonstrate that, in agreement with data from human tumors, p63 plays a markedly different biological role in cancer than p53.