Search for signal factors involved in hepatocarcinogenesis associated with non-alcoholic steatohepatitis (NASH) in mice fed a choline-deficient, methionine-lowered, high fat, amino acid-defined diet (CDAA-HF-T(-))

Abstract

The present study searched for signal factors in the mechanism underlying our mouse model of NASH-hepatocarcinogenesis using CDAA-HF-T(-). In the liver of mice fed CDAA-HF-T(-) for 52 or 63 weeks, hepatocellular adenomas and carcinomas, and hemangiosarcomas were observed, and the Rho Family GTPase and IL-8 signaling were upregulated. IL-8 and its receptors were upregulated in the non-tumor liver tissue, while in the tumor, IL-8 was abundantly expressed, but its receptors were downregulated. It is suggested that IL-8 complicatedly regulates NASH-hepatocarcinogenesis.