EMSY promoted the growth and migration of ovarian cancer cells

Tumour Biol. 2015 Apr;36(4):3085-92. doi: 10.1007/s13277-014-2944-3. Epub 2014 Dec 16.

Abstract

Epithelial ovarian cancer is one of the most common and aggressive diseases among the female reproductive organ malignancies, and the molecular mechanism underlying this disease remains largely unknown. EMSY, a binding partner of BRCA2, has been reported to be amplified in ovarian cancer. However, the expression pattern and biological functions of EMSY in the progression of ovarian cancer are not fully understood. In this study, it was found that the expression of EMSY was significantly elevated in ovarian cancer samples compared to their adjacent normal tissues. Moreover, overexpression of EMSY promoted the growth and migration of ovarian cancer cells, while knocking down the expression of EMSY inhibited the growth, migration, and tumorigenesis of ovarian cancer cells in vitro and in vivo. Mechanistically, EMSY was found to interact with beta-catenin and activate beta-catenin/TCF signaling. Our study demonstrated that EMSY played an oncogenic role in the progression of ovarian cancer cells and EMSY might be a promising target for the treatment.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • BRCA2 Protein / genetics
  • BRCA2 Protein / metabolism
  • Cell Line, Tumor
  • Cell Movement / genetics*
  • Cell Proliferation / genetics*
  • Cell Transformation, Neoplastic / genetics
  • Female
  • Gene Expression Regulation, Neoplastic
  • Humans
  • Mice
  • Neoplasm Proteins / biosynthesis
  • Neoplasm Proteins / genetics*
  • Nuclear Proteins / biosynthesis
  • Nuclear Proteins / genetics*
  • Ovarian Neoplasms / genetics*
  • Ovarian Neoplasms / pathology
  • Repressor Proteins / biosynthesis
  • Repressor Proteins / genetics*
  • Signal Transduction / genetics
  • TCF Transcription Factors / genetics
  • beta Catenin / biosynthesis

Substances

  • BRCA2 Protein
  • EMSY protein, human
  • Neoplasm Proteins
  • Nuclear Proteins
  • Repressor Proteins
  • TCF Transcription Factors
  • beta Catenin