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Carcinogenesis. 2014 Aug;35(8):1855-62. doi: 10.1093/carcin/bgu109. Epub 2014 May 19.

Evidence for a role of E-cadherin in suppressing liver carcinogenesis in mice and men.

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Institute for Biotechnology and Molecular Animal Breeding, The Gene Center.
Institute for Biotechnology and Molecular Animal Breeding, The Gene Center, Department of Internal Medicine II and.
Laboratory for Functional Genome Analysis, The Gene Center, University of Munich, 81377 Munich, Germany.
Department of Surgery, University of Magdeburg, Magdeburg, Germany.
Institute of Pathology, University of Heidelberg, Heidelberg, Germany.
Institute of Pathology, University of Munich, 80337 Munich, Germany and.
Department of Internal Medicine II and.
Department of Internal Medicine II and German Cancer Consortium (DKTK) and the German Cancer Research Center, Heidelberg, Germany


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.

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