| First Author | Schneider MR | Year | 2014 |
| Journal | Carcinogenesis | Volume | 35 |
| Issue | 8 | Pages | 1855-62 |
| PubMed ID | 24840851 | Mgi Jnum | J:213221 |
| Mgi Id | MGI:5583912 | Doi | 10.1093/carcin/bgu109 |
| Citation | Schneider MR, et al. (2014) Evidence for a role of E-cadherin in suppressing liver carcinogenesis in mice and men. Carcinogenesis 35(8):1855-62 |
| abstractText | The cell adhesion molecule E-cadherin has critical functions in development and carcinogenesis. Impaired expression of E-cadherin has been associated with disrupted tissue homeostasis, progression of cancer and a worse patient prognosis. So far, the role of E-cadherin in homeostasis and carcinogenesis of the liver is not well understood. By use of a mouse model with liver-specific deletion of E-cadherin and administration of the carcinogen diethylnitrosamine, we demonstrate that loss of E-cadherin expression in hepatocytes results in acceleration of the growth of hepatocellular carcinoma (HCC). In contrast, liver regeneration is not disturbed in mice lacking E-cadherin expression in hepatocytes. In human HCC, we observed four different expression patterns of E-cadherin. Notably, atypical cytosolic expression of E-cadherin was positively correlated with a poorer patient prognosis. The median overall survival of patients with HCC expressing E-cadherin on the membrane only was 221 weeks (95% confidence interval: 51-391) compared with 131 weeks in patients with cytosolic expression (95% confidence interval: 71-191 weeks; P < 0.05). In conclusion, we demonstrate that impaired expression of E-cadherin promotes hepatocellular carcinogenesis and is associated with a worse prognosis in humans. |
