Abstract
Purpose: Alteration of liver function during pro- gression of hepatocellular carcinoma (HCC) and cirrhosis affects the serum glycoprotein pattern. In this study, the changes in the N-glycome in liver tis- sue from patients with hepatocellular carcinoma and cirrhosis caused by hepatitis B virus infection were investigated to find out the relationship between this maker and liver disease. Methods: Twenty patients, 11 with cirrhosis and 9 with hepatocellular carcinoma, and 15 healthy donors were involved in this study. Liver protein N-glycans were profiled using the DSA-FACE technique developed in our laboratory. To further analyze the fucosylation status of these liver glycans Western lectin blots of total liver proteins were performed using Aspergillus oryzae lectin (AOL) as probe, which is a carbohydrate- binding protein that recognizes specifically α-1,6-fu- cosylated glycans. Results: The N-glycome of liver proteins in patients with HBV related HCC and cirrhosis was analyzed. Compared with healthy donors, the N-glycome had significantly less (p < 0.05) high mannose (M8) in both groups of patients. The total core α-1,6-fucosy-lation in total liver glycoproteins was dramatically increased during the progress of hepatocellular carcinoma and cirrhosis compared to the controls. Conclusion: These results show that fucosylation not only increases in serum proteins but also in liver tissue itself of patients with HBV related HCC and cirrhosis.
Highlights
Hepatocellular carcinoma (HCC) is a primary cancer of the liver and is one of the leading causes of death worldwide [1]
Overlaying with N-glycan profiles of serum and RNase B, L1 migrated at the same site as NA2 and L2, and as high as mannose 8 (M8), while L3 run as high as mannose 9 (M9) and NA2F
Alteration of liver function during progression of hepatocellular carcinoma (HCC) and cirrhosis affects the metabolism of glycoproteins and their concentration and secretion [18]
Summary
Hepatocellular carcinoma (HCC) is a primary cancer of the liver and is one of the leading causes of death worldwide [1]. HCC arises most commonly in cirrhotic livers following infection with hepatitis B virus (HBV) or hepatitis C virus (HCV) [2,3]. HCC develops when a mutation in the cellular machinery causes the cell to replicate at a higher rate and/or results in the cell avoiding apoptosis. Chronic infections with HBV and/or HCV could evolve to malignancy by repeatedly causing the immune system to attack the liver cells. Though extensive research over the past decade has identified a number of molecular biomarkers as well as cellular networks and signaling pathways affected in liver cancer [4], the pathophysiology of HCC is not understood clearly, but underlying liver dysfunction is a known predisposing condition
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