p63 expression is associated with p53 loss in oral-esophageal epithelia of p53-deficient mice.
p63 expression is associated with p53 loss in oral-esophageal epithelia of p53-deficient mice.
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发表时间：
2001-09
期刊：
影响因子：
11.2
通讯作者：
Y. Suliman;Oliver G. Opitz;Anjali Narayan Avadhani;Timothy C. Burns;W. El-Deiry;David T.W. Wong;Anil K. Rustgi
中科院分区：
文献类型：
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作者：
Y. Suliman;Oliver G. Opitz;Anjali Narayan Avadhani;Timothy C. Burns;W. El-Deiry;David T.W. Wong;Anil K. Rustgi
p53基因家族，包括p53、p63和p73，具有重叠和独特的功能作用。这些成员具有结构相似性，允许在发育和关键细胞功能（如诱导细胞凋亡）中重要的基因激活中动态相互作用。而p53是一个经典的肿瘤抑制基因，p63和p73并不分享癌症的形成和发展的这一特点。这些成员的表达水平的补偿，在一个背景，是缺乏其中之一，以前没有检查。鉴于p63在口腔-食管复层鳞状上皮细胞的发育和分化中的重要性，以及p53缺失小鼠中口腔-食管肿瘤的缺失，我们假设并在本文中描述了p63表达与p53缺陷背景中p53的缺失相关。与野生型小鼠相比，p53基因缺失小鼠的口腔-食管上皮中p63的全长和氨基截短形式均表达并增加，并且p21的诱导可能通过p63的增加而被潜在地保留。
The p53 gene family, comprising p53, p63, and p73, has overlapping and distinctive functional roles. These members share structural similarities allowing for dynamic interplay in the activation of genes that are important in development and key cellular functions, such as the induction of apoptosis. Whereas p53 is a classical tumor suppressor gene, p63 and p73 do not share this feature in cancer formation and progression. The compensation in the expression level of these members in a background that is deficient for one of them has not been examined previously. Given the importance of p63 in the development and differentiation of oral-esophageal stratified squamous epithelia and the absence of oral-esophageal tumors in p53-null mice, we postulated and describe herein that p63 expression is associated with the loss of p53 in a p53-deficient background. Both full-length and amino-truncated forms of p63 are expressed and increased in oral-esophageal epithelia of p53-null mice when compared with wild-type mice, and the induction of p21 may potentially be preserved through the increase of p63.