p63 expression is associated with p53 loss in oral-esophageal epithelia ofp53-deficient mice

The p53 gene family, comprising p53, p63, and p73, has overlapping and dist inctive functional roles. These members share structural similarities allow ing 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 t he development and differentiation of oral-esophageal stratified squamous e pithelia and the absence of oral-esophageal tumors in p53-null mice, we pos tulated 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 p 53-null mice when compared with wild-type mice, and the induction of p21 ma y potentially be preserved through the increase of p63.