Expression of BVES in gallbladder carcinoma and inhibitory effects of its overexpression on proliferation and invasion of gallbladder carcinoma cells
10.3781/j.issn.1000-7431.2018.33.196
- Author:
Chengjian SHI
1
Author Information
1. Department of Biliary-Pancreatic Surgery, Tongji Hospital Affiliated to Tongji Medical College, Huazhong University of Science and Technology
- Publication Type:Journal Article
- Keywords:
Blood vessel epicardial substance;
Cell proliferation;
Gallbladder neoplasms;
Neoplasm invasiveness
- From:
Tumor
2018;38(10):958-964
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To investigate the expression of blood vessel epicardial substance (BVES) in gallbladder carcinoma and the effects of BVES overexpression on the proliferation and invasion of gallbladder cancer GBC-SD cells. Methods: Immunohistochemistry was used to detect the expression of BVES in gallbladder carcinoma tissues and the para-cancerous tissues. The BVES overexpressed lentivirus was infected into gallbladder cancer GBC-SD cells, while the GBC-SD cells infected with empty carrier lentivirus were used as the negative control, and the uninfected GBC-SD cells were used as the blank control. The expression of BVES protein in GBC-SD cells was detected by Western blotting. The proliferation and invasion of GBC-SD cells in different groups were detected by colony formation assay and Transwell assay, respectively. Results: The positive expression rate of BVES in the gallbladder carcinoma tissues was lower than that in the para-cancerous tissues (P < 0.01). The expression level of BVES protein in GBC-SD cells infected with BVES overexpressed lentivirus was higher than that in the negative control group or the blank control group (both P < 0.05). The proliferation and invasion abilities of GBC-SD cells after the infection of BVES overexpressed lentivirus were significantly decreased (both P < 0.05). Conclusion: The positive expression rate of BVES is low in gallbladder carcinoma. Overexpression of BVES can inhibit the proliferation and invasion of gallbladder carcinoma GBC-SD cells.