Downregulation of N-cadherin expression inhibits invasiveness, arrests cell cycle and induces cell apoptosis in esophageal squamous cell carcinoma

Cancer Invest. 2010 Jun;28(5):479-86. doi: 10.3109/07357900903476745.

Abstract

Some studies have demonstrated that N-cadherin is upregulated in more invasive cancer cell lines and tumors and plays a key role in intercellular adhesion. However, the understanding on the roles N-cadherin plays in esophageal squamous cell carcinoma (ESCC) is still poor. Our data showed that knock-down of N-cadherin in ESCC cell line (EC9706) could arrest cell cycle at G0/G1 phase, induce cell apoptosis, reduce the invasiveness in vitro, and inhibit the tumor formation in vivo. These results suggest that N-cadherin is an important factor in the progression and metastasis of ESCC and N-cadherin may serve as a potential molecular target for biotherapy of ESCC.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antigens, CD / metabolism*
  • Apoptosis / genetics
  • Cadherins / metabolism*
  • Carcinoma, Squamous Cell / metabolism*
  • Carcinoma, Squamous Cell / pathology
  • Cell Cycle / genetics
  • Cell Line, Tumor
  • Cell Proliferation
  • Disease Progression
  • Down-Regulation
  • Esophageal Neoplasms / metabolism*
  • Esophageal Neoplasms / pathology
  • Humans
  • Matrix Metalloproteinase 9 / metabolism
  • Mice
  • Mice, Inbred BALB C
  • Mice, Nude
  • Neoplasm Invasiveness
  • Neoplasm Transplantation

Substances

  • Antigens, CD
  • CDH2 protein, human
  • Cadherins
  • Matrix Metalloproteinase 9