Skin human papillomavirus type 38 alters p53 functions by accumulation of ΔNp73

摘要: The E6 and E7 of the cutaneous human papillomavirus (HPV) type 38 immortalize primary keratinocytes, an event normally associated with inactivation pathways controlled by tumour suppressor p53. Here, we show for first time that HPV38 alters p53 functions. Expression in keratinocytes or skin transgenic mice induces stabilization wild-type This selectively activates transcription ΔNp73, isoform p53-related protein p73, which turn inhibits capacity to induce genes involved growth suppression apoptosis. ΔNp73 downregulation antisense oligonucleotide leads transcriptional re-activation p53-regulated Our findings illustrate a novel mechanism alteration function is mediated HPV support role carcinogenesis.