Aberrant expression of Golgi protein 73 is indicative of a poor outcome in hepatocellular carcinoma

Golgi protein 73 (GP73), a resident Golgi type-II membrane protein, is often upregulated in hepatocytes. In the present study, shRNA-mediated suppression of GP73 expression in hepatocellular carcinoma (HCC) cell lines (MHCC97H, HCCLM3) resulted in a significant inhibition of cell motility and invasion and also led to the regression of epithelial-mesenchymal transition phenotypes. In contrast, overexpression of GP73 in the SMMC7721 cell line retrieved the expression of EMT markers, and promoted cell motility and invasion. High expression of GP73 was also found in HCC tissues with metastasis, as detected by western blot and immunohistochemistry analyses. Kaplan-Meier survival analysis showed that the survival of patients with high GP73 expression was significantly poorer than that of patients with low GP73 expression (p=0.027). Our findings demonstrated an important role of GP73 in HCC metastasis, and indicated that GP73 is a candidate target for HCC therapy.