Loss of ΔNp63α promotes mitotic exit in epithelial cells

FEBS Lett. 2011 Sep 2;585(17):2720-6. doi: 10.1016/j.febslet.2011.07.030. Epub 2011 Aug 3.

Abstract

Protein p63 is a key regulator in cell proliferation and cell differentiation in stratified squamous epithelium. ΔNp63α is the most commonly expressed p63 isoform, which is often overexpressed in human tumor. In the present work we report the potential involvement of ΔNp63α in cell cycle regulation. ΔNp63α accumulated in mitotic cells but its expression decreased during mitotic exit. Moreover, ΔNp63α knockdown promoted mitotic exit. ΔNp63α shares a conserved destruction box (D-box) motif with other potential targets of the Anaphase-Promoting Complex/Cyclosome (APC/C). Overexpression of APC/C coactivator Cdh1 destabilized ΔNp63α. Our results suggest that ΔNp63α level is cell cycle-regulated and may play a role in the regulation of mitotic exit.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cell Line, Tumor
  • Epithelial Cells / cytology*
  • Epithelial Cells / metabolism*
  • HeLa Cells
  • Humans
  • Immunoblotting
  • Mitosis / genetics
  • Mitosis / physiology*
  • Protein Isoforms / genetics
  • Protein Isoforms / metabolism*
  • RNA, Small Interfering / genetics
  • Transcription Factors / genetics
  • Transcription Factors / metabolism*
  • Tumor Suppressor Proteins / genetics
  • Tumor Suppressor Proteins / metabolism*

Substances

  • Protein Isoforms
  • RNA, Small Interfering
  • TP63 protein, human
  • Transcription Factors
  • Tumor Suppressor Proteins