Downregulated expression of hepatoma-derived growth factor (HDGF) reduces gallbladder cancer cell proliferation and invasion

• DOI: 10.1007/s12032-013-0587-7
• Publication Date: 2013-04-22T06:34:57Z
• Authors: Maolan Li; Jun Shen; Xiangsong Wu; Bingtai Zhang; Rui Zhang; Hao Weng; Qian Ding; Zhujun Tan; Guofeng Gao; Jiasheng Mu; Jiahua Yang; Yijun Shu; Runfa Bao; Qichen Ding; Wenguang Wu; Yang Cao; Yingbin Liu
• Keywords: Cell Nucleus; Male; 0301 basic medicine; Chi-Square Distribution; Down-Regulation; Cell Growth Processes; Kaplan-Meier Estimate; Middle Aged; Immunohistochemistry; 3. Good health; 03 medical and health sciences; Treatment Outcome; Cell Line, Tumor; Multivariate Analysis; Humans; Intercellular Signaling Peptides and Proteins; Female; Gallbladder Neoplasms; Neoplasm Invasiveness; RNA Interference

Hepatoma-derived growth factor (HDGF), a heparin-binding growth factor, has a wide range of biological functions, including mitogenic activity and vascular development. Recent studies demonstrated that HDGF also acted as an oncogene with aberrantly increased activity in multiple human cancers; however, little is known about the biological function of HDGF in gallbladder cancer (GBC). In this study, we focused on the clinical significance and biological functions of HDGF in GBC and found that Nuclear HDGF protein overexpression was frequently detected in GBC tissues. Patients with nuclear HDGF-positive tumors had worse overall survival than patients with HDGF-negative tumors. Furthermore, treatment of GBC lines with HDGF-targeting siRNA oligonucleotides (HDGF-siRNA) significantly reduced the proliferation of GBC-SD and SGC-996 cell lines and diminished both anchorage-independent growth on soft agar and cell migration. These data indicate that HDGF acts as a putative oncogene in GBC and could be a novel diagnostic and therapeutic target for GBC.