SOX 1, contrary to SOX 2, suppresses proliferation, migration, and invasion in human laryngeal squamous cell carcinoma by inhibiting the Wnt/β-catenin pathway

Tumour Biol. 2015 Nov;36(11):8625-35. doi: 10.1007/s13277-015-3389-z. Epub 2015 Jun 4.

Abstract

Sex-determining region Y (SRY)-box protein 1 (SOX 1) has been reported to have the inhibiting effects on various cancer cells; however, the expression and effect of SOX 1 on laryngeal squamous cell carcinoma (LSCC) have not been determined. Therefore, the aim of this study was to assess the anti-proliferation and metastatic effects of SOX 1 and its related mechanisms on LSCC. According to our present study, first, we found that overexpression of SOX 1 could significantly inhibit proliferation and promote apoptosis in Tu212 cells. Additionally, overexpression of SOX 1 suppressed the migration and invasion potential of Tu212 cells via regulating Wnt/β-catenin pathway. Finally, we demonstrated for the first time that overexpression of SOX 1 could downregulate the expression of SOX 2, and co-expression of SOX 1 and SOX 2 could reverse the anti-tumor effect of SOX 1. In conclusion, our studies suggested that SOX 1 suppressed cell growth and invasion in Tu212 cells by inhibiting Wnt/β-catenin pathway, and the anti-tumor effect of SOX 1 could be weakened by SOX 2, which may be a potential molecular basis for clinical treatment of LSCC.

Keywords: Apoptosis; LSCC; Metastasis; SOX 1; SOX 2; Wnt/β-catenin.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Apoptosis
  • Carcinoma, Squamous Cell / genetics*
  • Carcinoma, Squamous Cell / pathology
  • Cell Line, Tumor
  • Cell Movement / genetics
  • Cell Proliferation / genetics
  • Gene Expression Regulation, Neoplastic
  • Humans
  • Laryngeal Neoplasms / genetics*
  • Laryngeal Neoplasms / pathology
  • Neoplasm Invasiveness / genetics
  • Neoplasm Metastasis
  • SOXB1 Transcription Factors / biosynthesis*
  • SOXB1 Transcription Factors / genetics
  • Wnt Signaling Pathway

Substances

  • SOXB1 Transcription Factors