Expression of Hu-IFN-alpha R2 chain of Type I interferon receptor in humanhepatocellular carcinoma and non-cancerous tissues

Type I interferon (IFN) receptor consists of two chains (Hu-IFN-alpha R1 an d Hu-IFN-alpha R2), and Hu-IFN-alpha R2 takes a soluble, short, or long for m (Hu-IFN-alpha R2a, Hu-IFN-alpha R2b, or Hu-IFN-alpha R2c, respectively). We examined Hu-IFN-alpha R2 expression in hepatocellular carcinoma (HCC) ti ssues and their corresponding non-cancerous (non-HCC) tissues. Immunohistoc hemically, Hu-IFN-alpha R2 expression was positive in 53 (77%) of 69 HCC ti ssues and in 61 (88%) of 68 non-HCC tissues. Hu-IFN-alpha R2 protein in tis sue homogenates of HCC and non-HCC tissues obtained from 29 patients was me asured by using ELISA kits, and the amount was 12.7+/-10.9 pg/mg protein in HCC tissue and 10.5+/-5.0 pg/mg protein in non-HCC tissue. Number of speci mens in which Hu-IFN-alpha R2 level was 3 pg/mg protein or lower, or 20 pg/ mg protein or higher, was one each for non-HCC, while it was 7 (24%) and 6 (21%) for HCC. RT-PCR analysis was done in 7 of the 29 HCC cases. It reveal ed both Hu-IFN-alpha R2a and Hu-IFN-alpha R2c were expressed in all HCC tis sues and in 4 of the 7 non-HCC tissues, and Hu-IFN-alpha R2b was expressed in all HCC tissues and in 4 of the 7 non-HCC tissues. Because immunostainin g intensity of Hu-IFN-alpha R2 tended to be higher in the areas with active inflammation, effects of inflammatory cytokines (IL-1 alpha, IL-1 beta, an d TNF-alpha on Hu-IFN-alpha R2 expression were examined on 11 HCC cell line s. As a result, TNF-alpha up-regulated Hu-IFN-alpha R2 expression in 7 of t he 11 cell lines. In 3 of the 7 cell lines, up-regulation of Hu-IFN-alpha R 2 on cell surface, as well as of the soluble form of Hu-IFN-alpha R2, was i nduced not only by TNF-alpha, but also by IL-1 alpha or IL-1 beta. In concl usion, both HCC and non-HCC tissues frequently express Hu-IFN-alpha R2c tha t is necessary for Type I IFN response. Hu-IFN-alpha R2 expression in HCC t issues is often attenuated or enhanced, and may be regulated by inflammator y cytokines.