BACKGROUND/AIMS: Hepsin is a type II transmembrane protein predominantly expressed in the liver and has been implicated in participation in blood coagulation pathway and epithelial carcinogenesis. The aim of this current study is to investigate the role of hepsin in hepatocarcinogenesis. METHODS: Quantitative real-time RT-PCR was used to investigate the expression levels of hepsin in a total of 50 paired hepatocellular carcinomas (HCCs) and the corresponding non-tumor liver tissues. Hepsin was transfected to the hepsin-non-expressing SK-HEP-1 cells to study the change of cell proliferation. RESULTS: In 62% (31/50) patients, the expression levels of hepsin in non-tumor liver tissues are at least twofold higher than those in the corresponding HCC tissues. Positive hepatitis B surface antigen was more often detected in patients with hepsin underexpressed in the HCC tissues (74.2% vs. 31.6%, P=0.007). Patients with hepsin underexpressed in the HCC tissues survived shorter time than those without hepsin underexpression in the HCC tissues. The cell proliferation and for a colony formation of SK-HEP-1 HCC cells were inhibited by hepsin. CONCLUSIONS: Most HCC patients had hepsin underexpressed in the HCC tissues. These patients survived for a shorter time compared with those without hepsin underexpression in the HCC tissues. Hepsin expression could inhibit cell proliferation and colony formation of HCC cells.
BACKGROUND/AIMS: Hepsin is a type II transmembrane protein predominantly expressed in the liver and has been implicated in participation in blood coagulation pathway and epithelial carcinogenesis. The aim of this current study is to investigate the role of hepsin in hepatocarcinogenesis. METHODS: Quantitative real-time RT-PCR was used to investigate the expression levels of hepsin in a total of 50 paired hepatocellular carcinomas (HCCs) and the corresponding non-tumor liver tissues. Hepsin was transfected to the hepsin-non-expressing SK-HEP-1 cells to study the change of cell proliferation. RESULTS: In 62% (31/50) patients, the expression levels of hepsin in non-tumor liver tissues are at least twofold higher than those in the corresponding HCC tissues. Positive hepatitis B surface antigen was more often detected in patients with hepsin underexpressed in the HCC tissues (74.2% vs. 31.6%, P=0.007). Patients with hepsin underexpressed in the HCC tissues survived shorter time than those without hepsin underexpression in the HCC tissues. The cell proliferation and for a colony formation of SK-HEP-1 HCC cells were inhibited by hepsin. CONCLUSIONS: Most HCC patients had hepsin underexpressed in the HCC tissues. These patients survived for a shorter time compared with those without hepsin underexpression in the HCC tissues. Hepsin expression could inhibit cell proliferation and colony formation of HCC cells.