Ke Li1, Xin Wang, Wei He, Na Lin, Qing-Xia Fan. 1. Department of Oncology, First Affiliated Hospital, Zhengzhou University, Zhengzhou, Henan, PR China.
Abstract
BACKGROUND AND OBJECTIVE: E- and N-cadherin are calcium-dependent cell adhesion molecules that mediate cell-cell adhesion and also modulate cell migration and tumor invasion. It has been suggested that, unlike E-cadherin, N-cadherin may promote invasion and metastasis of carcinoma. This study was to explore the correlation of E-cadherin and N-cadherin expression to clinicopathologic features of esophageal squamous cell carcinoma (ESCC), and to investigate the effect of silencing N-cadherin expression by RNA interference (RNAi) on the invasiveness of EC9706 cells. METHODS: PV immunohistochemistry was used to detect the expression of E-cadherin and N-cadherin in 62 specimens of normal esophageal epithelium, 31 specimens of adjacent atypical hyperplasia epithelium and 62 specimens of ESCC. N-cadherin siRNA was transfected into EC9706 cells, and the effect of RNAi was assessed by RT-PCR and Western blot. The invasiveness of EC9706 cells was determined by Transwell chamber assay. RESULTS: The positive rates of E-cadherin and N-cadherin were 95.2% and 29.0% in normal esophageal epithelium, 71.0% and 61.3% in adjacent atypical hyperplasia epithelium, 40.3% and 75.8% in ESCC. The negativity of E-cadherin and positivity of N-cadherin were correlated to invasion, differentiation, and lymph node metastasis of ESCC (p < 0.05). E-cadherin expression was negatively correlated to N-cadherin expression in ESCC (gamma = -0. 534, p < 0.05). N-cadherin RNAi significantly inhibited N-cadherin expression in EC9706 cells, and decreased the number of EC9706 cells that invaded through the basement membrane from (123.40 +/- 8.23) to (49.60 +/- 6.80) (p < 0.05). CONCLUSIONS: Down-regulation of E-cadherin and up-regulation of N-cadherin may be involved in the genesis of ESCC. Silencing N-cadherin using RNA interference could inhibit the invasiveness of EC9706 cells in vitro.
BACKGROUND AND OBJECTIVE: E- and N-cadherin are calcium-dependent cell adhesion molecules that mediate cell-cell adhesion and also modulate cell migration and tumor invasion. It has been suggested that, unlike E-cadherin, N-cadherin may promote invasion and metastasis of carcinoma. This study was to explore the correlation of E-cadherin and N-cadherin expression to clinicopathologic features of esophageal squamous cell carcinoma (ESCC), and to investigate the effect of silencing N-cadherin expression by RNA interference (RNAi) on the invasiveness of EC9706 cells. METHODS: PV immunohistochemistry was used to detect the expression of E-cadherin and N-cadherin in 62 specimens of normal esophageal epithelium, 31 specimens of adjacent atypical hyperplasia epithelium and 62 specimens of ESCC. N-cadherin siRNA was transfected into EC9706 cells, and the effect of RNAi was assessed by RT-PCR and Western blot. The invasiveness of EC9706 cells was determined by Transwell chamber assay. RESULTS: The positive rates of E-cadherin and N-cadherin were 95.2% and 29.0% in normal esophageal epithelium, 71.0% and 61.3% in adjacent atypical hyperplasia epithelium, 40.3% and 75.8% in ESCC. The negativity of E-cadherin and positivity of N-cadherin were correlated to invasion, differentiation, and lymph node metastasis of ESCC (p < 0.05). E-cadherin expression was negatively correlated to N-cadherin expression in ESCC (gamma = -0. 534, p < 0.05). N-cadherin RNAi significantly inhibited N-cadherin expression in EC9706 cells, and decreased the number of EC9706 cells that invaded through the basement membrane from (123.40 +/- 8.23) to (49.60 +/- 6.80) (p < 0.05). CONCLUSIONS: Down-regulation of E-cadherin and up-regulation of N-cadherin may be involved in the genesis of ESCC. Silencing N-cadherin using RNA interference could inhibit the invasiveness of EC9706 cells in vitro.