BACKGROUND: Beta-catenin has two distinct roles in E-cadherin mediated cell adhesion and carcinogenesis by activating the wnt/beta-catenin signaling pathway. One occurs at the cell-adhesion site, where cadherins are linked to the actin-based cytoskeleton. The other takes place in the cytoplasm and nuclei and is thought to regulate cell transformation. We studied the role of beta-catenin in hepatocarcinogenesis of rats. METHODS: Fresh liver specimens were obtained from normal rats, and atypical hyperplasia livers and hepatocarcinoma tissues from model rats. The changes of beta-catenin in gene expression levels were detected by reverse transcriptase polymerase chain reaction (RT-PCR) in the different specimens separately. At the same time, their localization was observed immunohistochemically. RESULTS: In the normal liver specimens, beta-catenin staining was seen in the cell membrane. In liver specimens of atypical hyperplasia, beta-catenin staining occurred in the cell cytoplasm of some cells as well as in the cell membrane of others. Immunohistochemically cancerous tissues showed the presence of beta-catenin in the cytoplasm and nuclei. RT-PCR revealed that the gene expression levels of beta-catenin were same in all samples. CONCLUSIONS: The accumulation of beta-catenin in the cytoplasm and/or nuclei frequently occurs in hepatocarcinogenesis of rats. It may be an early event in the development of hepatocarcinoma of rats.
BACKGROUND:Beta-catenin has two distinct roles in E-cadherin mediated cell adhesion and carcinogenesis by activating the wnt/beta-catenin signaling pathway. One occurs at the cell-adhesion site, where cadherins are linked to the actin-based cytoskeleton. The other takes place in the cytoplasm and nuclei and is thought to regulate cell transformation. We studied the role of beta-catenin in hepatocarcinogenesis of rats. METHODS: Fresh liver specimens were obtained from normal rats, and atypical hyperplasia livers and hepatocarcinoma tissues from model rats. The changes of beta-catenin in gene expression levels were detected by reverse transcriptase polymerase chain reaction (RT-PCR) in the different specimens separately. At the same time, their localization was observed immunohistochemically. RESULTS: In the normal liver specimens, beta-catenin staining was seen in the cell membrane. In liver specimens of atypical hyperplasia, beta-catenin staining occurred in the cell cytoplasm of some cells as well as in the cell membrane of others. Immunohistochemically cancerous tissues showed the presence of beta-catenin in the cytoplasm and nuclei. RT-PCR revealed that the gene expression levels of beta-catenin were same in all samples. CONCLUSIONS: The accumulation of beta-catenin in the cytoplasm and/or nuclei frequently occurs in hepatocarcinogenesis of rats. It may be an early event in the development of hepatocarcinoma of rats.