¹Department of Surgery, Saga Medical School, 5-1-1 Nabeshima, Saga 849-8501, Japan

Correspondence: K Miyazaki, E-mail: miyazak2@post.saga-med.ac.jp

Received 27 July 2001; Revised 18 October 2001; Accepted 22 October 2001.

Abstract

Hepatocellular carcinoma is a well-known malignancy in the world. However, the molecular mechanism of carcinogenesis and tumour progression remains unclear. Recently, reduced E-cadherin expression due to transcriptional suppressor Snail was proven in a panel of epithelial and dedifferentiated cells derived from carcinomas of various etiologies. In the present study, we examined Snail and E-cadherin mRNA/protein expression in five hepatocellular carcinoma cell lines with variable phenotypes (HuL-1, Hep-G₂, Changliver, HLE, and HLF). The results demonstrated that the presence of Snail mRNA in HuL-1, Changliver, HLE and HLF cells detected by RT–PCR, which was further proven by in situ hybridization in tumours induced by HuL-1, Changliver, and HLF cells where Snail mRNA signals expressed in each of the sections. By contrast, E-cadherin mRNA and protein expression were only detected in Hep-G₂ cells by RT–PCR and Western blot, respectively. These results were also consistent with the data obtained from in vivo immunohistochemical staining where membranous expression of endogenous E-cadherin protein was revealed only in tumour sections induced by Hep-G₂ cells. Here we are the first to report that there is an inverse correlation between Snail and E-cadherin expression in HCC cells as well.