Ndc80 gene silencing inhibits the proliferation, migration and invasion of human gallbladder carcinoma cells
10.3781/j.issn.1000-7431.2020.11.008
- Author:
Zexu CHEN
1
Author Information
1. The First Clinical Medical School, Shanxi Medical University
- Publication Type:Journal Article
- Keywords:
Cell movement;
Cell proliferation;
Gallbladder neoplasms;
Nuclear division cycle 80
- From:
Tumor
2020;40(4):266-275
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To investigate the effects of silencing nuclear division cycle 80 (NDC 80) gene expression on the proliferation, migration and invasion abilities of human gallbladder carcinoma GBC-SD and NOZ cells. Methods: Real-time fluorescent quantitative PCR and Western blotting were used to detect the expressions of NDC80 mRNA and protein in gallbladder carcinoma GBC-SD and NOZ cells after the transfection of NDC80 siRNA, respectively. After NDC80 gene silencing, the proliferation of GBC-SD and NOZ cells were detected by CCK-8 test and clone formation test, respectively. Transwell chamber assay was used to detect the migration and invasion abilities of gallbladder carcinoma cells after NDC80 gene silencing. Results: The NDC80 siRNA (si-NDC80 group) and the negative control (si-NC group) were successfully transfected into gallbladder carcinoma GBC-SD and NOZ cells, respectively. The expression levels of NDC80 mRNA and proteins in GBC-SD and NOZ cells transfected with si-NDC80 were significantly lower than those in si-NC group (all P < 0.001). Compared with the si-NC group, si-NDC80 transfection reduced the proliferation and clone formation abilities of GBC-SD and NOZ cells (all P < 0.001), and the migration and invasion abilities of GBC-SD and NOZ cells transfected with si-NDC80 were significantly decreased (all P < 0.001). Conclusion: Silencing the expression of NDC80 gene can inhibit the proliferation, migration and invasion of human gallbladder carcinoma cells, suggesting that NDC80 plays an important role in the occurrence and development of gallbladder carcinoma.