Suppression of nasopharyngeal carcinoma cell by targeting β-catenin signaling pathway

Cancer Epidemiol. 2012 Apr;36(2):e116-21. doi: 10.1016/j.canep.2011.11.002. Epub 2011 Dec 4.

Abstract

Aim: To investigate the role of β-catenin in pathogenesis of nasopharyngeal carcinoma (NPC).

Methods: Cellular proliferation, apoptosis, matrix penetration assay, and western blotting were employed to determine cell biological changes in NPC cell lines transfected with β-catenin siRNA. Immunohistochemistry staining was used to detect β-catenin and Ki-67 expression in NPC tissue.

Results: β-Catenin was upregulated in NPC cell lines and tissues compared with chronic nasopharyngitis tissue. β-Catenin knockdown dramatically inhibited cellular growth, migration and invasion, but induced apoptosis of NPC cells. Further study showed that downstream genes of β-catenin signaling pathway including cyclin D1, c-Myc, MMP2 and MMP9 expression were suppressed in NPC cell lines transfected with β-catenin siRNA.

Conclusion: Targeting β-catenin signaling pathway may be a noval strategy for NPC therapy.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Adult
  • Aged
  • Blotting, Western
  • Carcinoma
  • Female
  • Gene Knockdown Techniques
  • Humans
  • Immunohistochemistry
  • Male
  • Middle Aged
  • Nasopharyngeal Carcinoma
  • Nasopharyngeal Neoplasms / metabolism*
  • RNA, Small Interfering
  • Signal Transduction / physiology*
  • Transfection
  • Up-Regulation
  • Young Adult
  • beta Catenin / metabolism*

Substances

  • CTNNB1 protein, human
  • RNA, Small Interfering
  • beta Catenin