SOX2 enhances the migration and invasion of ovarian cancer cells via Src kinase

PLoS One. 2014 Jun 17;9(6):e99594. doi: 10.1371/journal.pone.0099594. eCollection 2014.

Abstract

Ovarian cancer is the leading cause of death among gynecologic cancers and is the fifth leading cause of all cancer-related deaths among women. The development of novel molecular targets is therefore important to many patients. Recently, the SRY-related transcription factor SOX2 has been widely reported to be involved in multiple pathophysiological diseases, including maintenance of stem cell characteristics and carcinogenesis. Up to now, SOX2 has been mainly shown to promote the development of cancer, although its inhibitory roles in cancer have also been reported. However, the role of SOX2 in ovarian cancer is largely unknown. In the present study, we detected the expression of SOX2 in 64 human serous ovarian carcinoma (SOC) tissues and paired corresponding metastatic specimens using immunohistochemistry. The results showed that the expression of SOX2 in primary tumors is much lower than that in the corresponding metastatic lesions. We further found that SOX2 overexpression promotes proliferation, migration and invasion, while inhibiting adhesion abilities of SOC cells. Finally, we found that SOX2 targets Src kinase, a non-receptor tyrosine kinase that regulates cell migration, invasion and adhesion in SOC cells. Together, these results suggested that Src kinase is a key molecule in SOX2-mediated migration and invasion of SOC cells.

Publication types

  • Research Support, Non-U.S. Gov't
  • Retracted Publication

MeSH terms

  • Adult
  • Aged
  • Aged, 80 and over
  • Cell Adhesion
  • Cell Line, Tumor
  • Cell Movement*
  • Cell Proliferation
  • Cystadenocarcinoma, Serous / metabolism*
  • Cystadenocarcinoma, Serous / secondary
  • Female
  • Gene Expression
  • Humans
  • Middle Aged
  • Neoplasm Invasiveness
  • Ovarian Neoplasms / enzymology
  • Ovarian Neoplasms / metabolism*
  • Ovarian Neoplasms / pathology
  • Peritoneal Neoplasms / metabolism*
  • Peritoneal Neoplasms / secondary
  • Phosphorylation
  • Protein Processing, Post-Translational
  • SOXB1 Transcription Factors / physiology*
  • src-Family Kinases / metabolism*

Substances

  • SOX2 protein, human
  • SOXB1 Transcription Factors
  • src-Family Kinases

Grants and funding

The study was supported by grants from the National Natural Science Foundation of China (NSFC No. 81272883, No. 81020108027 and No. 81172478). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.