Upregulation of Glycoprotein Nonmetastatic B by Colony-Stimulating Factor-1 and Epithelial Cell Adhesion Molecule in Hepatocellular Carcinoma Cells
Upregulation of Glycoprotein Nonmetastatic B by Colony-Stimulating Factor-1 and Epithelial Cell Adhesion Molecule in Hepatocellular Carcinoma Cells
复制标题
集落刺激因子 1 和上皮细胞粘附分子对肝细胞癌细胞中糖蛋白非转移性 B 的上调
DOI:
10.3727/096504013x13657689382851
复制
发表时间:
2012-01-01
影响因子:
3.1
通讯作者:
Chang, Hulin
中科院分区:
文献类型:
--
作者:
Tian, Feng;Liu, Chang;Chang, Hulin
Considerable effort has been made in elucidating the appropriate biomarkers and the mechanism and functional significance of these biomarkers in hepatocellular carcinoma (HCC). Glycoprotein nonmetastatic B (GPNMB) overexpression occurs in cutaneous melanomas and breast cancer, and it is an attractive candidate for cancer therapy. However, little is known about the expression and regulation of GPNMB in HCC. In this study, we investigated the expression of GPNMB in HCC histochemically and tested the regulation effects of the epithelial cell adhesion molecule (EpCAM) and colony-stimulating factor (CSF-1) on the expression of GPNMB in HCC cells. Our results demonstrated that GPNMB levels were significantly enhanced in HCC compared with adjacent normal liver tissues. In HCC cells, GPNMB expression was regulated by EpCAM and CSF-1 partly through their common downstream product c-myc. Taken together, these results suggest that GPNMB, the expression of which was regulated in HCC cells by the highly coordinated function of various proteins, may be a potential target for HCC therapy.