DNA damage induces expression of WWP1 to target ΔNp63α to degradation

PLoS One. 2017 Apr 20;12(4):e0176142. doi: 10.1371/journal.pone.0176142. eCollection 2017.

Abstract

ΔNp63αplays key roles in cell survival and proliferation. So its expression is always tightly controlled in cells. We previously reported that DNA damage down-regulates transcription of ΔNp63αin FaDu and HaCat cells, which contributes to cell apoptosis. In the present study, we found that DNA damage induces down-regulation of ΔNp63αvia facilitating its proteasomal degradation in cell lines such as MDA-MB-231 and MCF10A. Further investigation revealed that transcription of WWP1 is stimulated by DNA damage in these cells. Knock-down of WWP1 abrogates DNA damage-induced down-regulation of ΔNp63αand partially rescues cell apoptosis. Interestingly, DNA damage may stimulate WWP1 through different mechanisms in different cell types: it up-regulates transcription of WWP1 in a p53-dependent manner in MCF10A and HEK293 cells, while miR-452 may be involved in DNA damage-induced up-regulation of WWP1 in MDA-MB-231 cells. Our study demonstrates a novel pathway which regulates ΔNp63αupon cellular response to chemotherapeutic agents.

MeSH terms

  • Cell Line, Tumor
  • DNA Damage*
  • Gene Knockdown Techniques
  • Genes, p53
  • HEK293 Cells
  • Humans
  • MicroRNAs / genetics
  • Proteasome Endopeptidase Complex / metabolism
  • Proteolysis
  • Transcription Factors / metabolism*
  • Transcription, Genetic
  • Tumor Suppressor Proteins / metabolism*
  • Ubiquitin-Protein Ligases / genetics
  • Ubiquitin-Protein Ligases / metabolism*
  • Up-Regulation

Substances

  • MIRN452 microRNA, human
  • MicroRNAs
  • TP63 protein, human
  • Transcription Factors
  • Tumor Suppressor Proteins
  • WWP1 protein, human
  • Ubiquitin-Protein Ligases
  • Proteasome Endopeptidase Complex

Grants and funding

This work was supported by National Natural Science Foundation of China (#31671423) and and Science and Technology Department of Sichuan Province (#2016JY0152). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.