O218 E-CADHERIN EXPRESSION CORRELATES WITH PROGRESSION OF ESOPHAGEAL SQUAMOUS CELL CARCINOMA

• Published in: Diseases of the esophagus 2019-11, Vol.32 (Supplement_2)
• Main Authors: Koda, Hanako, Yamada, Kazuhiko, Terayama, Masayoshi, Ryusuke, Sumiya, Nohara, Kyoko, Enomoto, Naoki, Kataoka, Atsuko, Mita, Hideaki, Takemura, Nobuyuki, Kiyomatsu, Tomomitsu, Kokudo, Norihiro, Kawamura, Yuki I
• Format: Article
• Language: English
• ISSN: 1442-2050; 1442-2050
• DOI: 10.1093/dote/doz092.218

Abstract Background & Aim E-cadherin is a member of the cadherin family and plays a major role in cell–cell adhesion of normal epithelium. Decreased or lack of E-cadherin expression has been reported in breast, colon and bladder cancer, and the disruption of the E-cadherin-mediated cell–cell adhesion is considered the first crucial step of metastasis. The esophageal stratified epithelial cells have many spines that intermingle with each other through desmosomes, in which E-cadherins play an important role for cell–cell adhesion. However, the significance of E-cadherin expression in the progression of esophageal squamous cell carcinoma (ESCC) still remains to be clarified. In the present study, we investigated the relation between E-cadherin expression in tumors and the clinicopathological features of ESCC. Method E-cadherin expression was evaluated in ESCC specimens of 61 patients who underwent surgery from April 2008 to December 2015 at the National Center for Global Health and Medicine by immunohistochemical staining. Distribution of E-cadherin in cancerous tissues was classified as Preserved (expression in cell membrane alone) or Disturbed (expression in cytoplasm or decreased/lack of expression of E-cadherin). Significance of the distribution pattern was analyzed by comparison to clinicopathological features. Results Thirty-seven of 61 (61%) cases revealed Preserved expression pattern while Disturbed distribution was observed in 24 of 61 (39%) cases. Compared to Preserved pattern, Disturbed expression of E-cadherin in tumors was significantly associated with advanced TNM stages (P=0.0462). Conclusion E-cadherin was expressed in most cases of ESCC; however, its distribution was not restricted in membrane but in the cytoplasm of tumors. Disturbed expression of E-cadherin in tumors correlated with advanced stage of ESCC, suggesting that the disruption of the E-cadherin-mediated cell–cell adhesion may play an important role in the progression of ESCC.