The Preliminary Study Regarding Expression of Hepcidin in Hepatocellular Carcinoma after HBV Infection and its Mechanism

Objective To study the expression of Hepcidin and its receptor Ferroportin in hepatocellular carcinoma (HCC) after HBV infection, and explore initially its mechanism in the development and progression of hepatocellular carcinoma (HCC). Methods 1. We screen out randomly 20 cases of normal persons and 25 cases of HCC after HBV infection , respectively, as the control group and HCC group. 2. The expression of Hepcidin, BMP6, IL-6, sTfR and SF in serum were measured by enzyme-linked immunosorbent assay (ELISA). Analyze the correlation between Hepcidin and various variables and compare the difference between the 2 groups. 3. The expression of Hepcidin receptor Ferroportin in tumor tissue and para-carcinoma tissue as well as normal liver tissue were detected by immunohistochemistry. Analyze the correlation with AFP level, TNM staging, and HCC clinical staging. Results 1. Serum levels of Hepcidin, were significantly lower in HCC group than those in normal control group (P＜0.0), positively correlated with IL-6 and BMP6 in HBV-related HCC group (P＜0.05, r＞0.5), and negatively correlated with sTfR and SF (P＜0.05, r＞0.5). P＜0.0The expression of Ferroportin in HBV-related HCC was negatively correlated with HCC clinical staging（P＜0.05,P=0.01,r=-0.505）.Conclusion 1. Serum levels of Hepcidin, were significantly lower in HCC than those in normal people, while serum levels of sTfR was significantly higher, which bring about iron overloading in body .It promote the occurrence of HCC accordingly. 2.As Hepcidin receptor, Ferroportin expressed at a low level in the liver cancer tissues.3. The low level of Hepcidin in HCC may be associated with the inhibition of BMP / SMAD signaling pathway and JAK / STAT signaling pathway