S100A2 gene is a direct transcriptional target of p53 homologues during keratinocyte differentiation

E. Lapi, A. Iovino, G. Fontemaggi, A. R. Soliera, S. Iacovelli, A. Sacchi, G. Rechavi, D. Givol, G. Blandino*, S. Strano

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

34 Scopus citations


The p53 paralogues p73, p63 and their respective truncated isoforms have been shown to be critical regulators of developmental and differentiation processes. Indeed, both p73- and p63-deficient mice exhibit severe developmental defects. Here, we show that S100A2 gene, whose transcript and protein are induced during keratinocyte differentiation of HaCaT cells, is a direct transcriptional target of p73β and ΔNp63α and is required for proper keratinocyte differentiation. Transactivation assays reveal that p73β and ΔNp63α exert opposite transcriptional effects on S100A2 gene. While ΔNp63α is found in vivo onto S100A2 regulatory regions predominantly in proliferating cells, p73β is recruited in differentiating cells. Silencing of p73 impairs the induction of S100A2 during the differentiation of HaCaT cells. Moreover, silencing of p73 or S100A2 impairs the proper expression of keratinocyte differentiation markers. Of note, p53 family members do not trigger S100A2 gene expression in response to apoptotic doses of cisplatin and doxorubicin.

Original languageEnglish
Pages (from-to)3628-3637
Number of pages10
Issue number26
StatePublished - 22 Jun 2006
Externally publishedYes


FundersFunder number
EC FP6503576
Fondazione Telethon
Ministero della Salute
Associazione Italiana per la Ricerca sul Cancro


    • Differentiation
    • Keratinocytes
    • S100A2
    • Transcription
    • p63
    • p73


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