BACKGROUND AND OBJECTIVE: It has been proven that Ezrin protein may interact with E-cadherin protein and take part in metastasis of tumor cells. This study was to investigate the expressions of Ezrin and E-cadherin in esophageal squamous cell carcinoma (ESCC) and their relationship with the clinicopathologic factors, and analyze their diagnostic values for ESCC. METHODS: The expression of Ezrin and E-cadherin in 72 specimen of ESCC and the paracancer normal squamous epithelium was detected using tissue array with SP immunohistochemistry. Their correlations to the clinicopathologic factors were analyzed statistically. RESULTS: The positive rate of Ezrin was significantly higher in ESCC than in para-cancer normal squamous epithelium (90.7% vs. 46.0%, P < 0.001); the positive rate of E-cadherin was significantly lower in ESCC than in para-cancer normal squamous epithelium (27.6% vs. 97.4%, P < 0.001). Ezrin expression was related to the invasiveness and lymph node metastasis of ESCC (P < 0.05); E-cadherin expression was related to the differentiation and lymph node metastasis of ESCC (P < 0.05). The high expression of Ezrin was related to the low expression of E-cadherin (P < 0.05). CONCLUSION: The activation of Ezrin and the absence of E-cadherin contribute to the tumorigenesis and metastasis of ESCC.
BACKGROUND AND OBJECTIVE: It has been proven that Ezrin protein may interact with E-cadherin protein and take part in metastasis of tumor cells. This study was to investigate the expressions of Ezrin and E-cadherin in esophageal squamous cell carcinoma (ESCC) and their relationship with the clinicopathologic factors, and analyze their diagnostic values for ESCC. METHODS: The expression of Ezrin and E-cadherin in 72 specimen of ESCC and the paracancer normal squamous epithelium was detected using tissue array with SP immunohistochemistry. Their correlations to the clinicopathologic factors were analyzed statistically. RESULTS: The positive rate of Ezrin was significantly higher in ESCC than in para-cancer normal squamous epithelium (90.7% vs. 46.0%, P < 0.001); the positive rate of E-cadherin was significantly lower in ESCC than in para-cancer normal squamous epithelium (27.6% vs. 97.4%, P < 0.001). Ezrin expression was related to the invasiveness and lymph node metastasis of ESCC (P < 0.05); E-cadherin expression was related to the differentiation and lymph node metastasis of ESCC (P < 0.05). The high expression of Ezrin was related to the low expression of E-cadherin (P < 0.05). CONCLUSION: The activation of Ezrin and the absence of E-cadherin contribute to the tumorigenesis and metastasis of ESCC.
Authors: K Alexa Orr Gandy; Mohamad Adada; Daniel Canals; Brittany Carroll; Patrick Roddy; Yusuf A Hannun; Lina M Obeid Journal: FASEB J Date: 2013-04-29 Impact factor: 5.191
Authors: David S Liu; Sanne J M Hoefnagel; Oliver M Fisher; Kausilia K Krishnadath; Karen G Montgomery; Rita A Busuttil; Andrew J Colebatch; Matthew Read; Cuong P Duong; Wayne A Phillips; Nicholas J Clemons Journal: Oncotarget Date: 2016-12-13