Suppression of invasion and peritoneal carcinomatosis of ovarian cancer cells by overexpression of AP-2alpha

Oncogene. 2004 Jul 15;23(32):5496-504. doi: 10.1038/sj.onc.1207723.


A previous report demonstrated that AP-2alpha favors the survival of ovarian cancer patients by clinical findings. However, the functional roles of AP-2alpha in human ovarian cancers have not been determined. To clarify the roles, we overexpressed AP-2alpha in SKOV3 human ovarian cancer cells, which originally possess little AP-2alpha. AP-2alpha overexpression changed cell morphology from spindle to epithelioid type and suppressed cell proliferation and invasion, which would be partially correlated with decreased phosphorylation levels of the erbB2, Akt and ERK pathways, increased E-cadherin and reduced pro-matrix metalloproteinase-2 levels. Moreover, nude mice intraperitoneally injected with AP-2alpha-overexpressing cells survived longer than those with neo-transfected cells. The present data represent the first direct evidence that AP-2alpha plays a tumor suppressive role in ovarian cancer.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cadherins / metabolism
  • Carcinoma / metabolism*
  • Cell Division / physiology
  • DNA-Binding Proteins / genetics
  • DNA-Binding Proteins / metabolism*
  • Female
  • Humans
  • Matrix Metalloproteinases / metabolism
  • Mitogen-Activated Protein Kinases / metabolism
  • Neoplasm Invasiveness
  • Ovarian Neoplasms / metabolism*
  • Ovarian Neoplasms / pathology
  • Peritoneal Neoplasms / metabolism*
  • Phosphorylation
  • Protein-Serine-Threonine Kinases / metabolism
  • Proto-Oncogene Proteins / metabolism
  • Proto-Oncogene Proteins c-akt
  • Receptor, ErbB-2 / metabolism
  • Transcription Factor AP-2
  • Transcription Factors / genetics
  • Transcription Factors / metabolism*


  • Cadherins
  • DNA-Binding Proteins
  • Proto-Oncogene Proteins
  • TFAP2A protein, human
  • Transcription Factor AP-2
  • Transcription Factors
  • Receptor, ErbB-2
  • AKT1 protein, human
  • Protein-Serine-Threonine Kinases
  • Proto-Oncogene Proteins c-akt
  • Mitogen-Activated Protein Kinases
  • Matrix Metalloproteinases