Effects of MnSOD silence on in vitro tumorigenicity in NCI-H446 cells.
10.11817/j.issn.1672-7347.2018.06.002
- Author:
Qing YUAN
1
;
Min WEN
1
;
Xiang LI
1
;
Ling SHU
1
;
Jianguo CAO
1
;
Jiansong ZHANG
1
Author Information
1. Department of Basic Medicine, College of Medicine of Human Normal University, Changsha 410013, China.
- Publication Type:Journal Article
- MeSH:
Adenoviridae;
Carcinogenesis;
Cell Line, Tumor;
Humans;
In Vitro Techniques;
Lung Neoplasms;
etiology;
metabolism;
RNA Interference;
Receptors, Urokinase Plasminogen Activator;
genetics;
metabolism;
Small Cell Lung Carcinoma;
etiology;
metabolism;
Spheroids, Cellular;
pathology;
Superoxide Dismutase;
genetics;
metabolism;
Tumor Stem Cell Assay;
Up-Regulation
- From:
Journal of Central South University(Medical Sciences)
2018;43(6):583-588
- CountryChina
- Language:Chinese
-
Abstract:
To investigate the effect of manganese superoxide dismutase (MnSOD) silence on the in vitro tumorigenicity in human small cell lung cancer NCI-H446 cells and the underlying mechanisms.
Methods: Sphere formation cells from NCI-H446 cells were obtained by suspension culture, while the expression of MnSOD and urokinase type plasminogen activator (uPAR) was analyzed by Western blot. Silence of MnSOD was performed by adenovirus infection in the second passage formation cells, and the effect of MnSOD silence on tumorigenicity in NCI-H446 cells was evaluated by sphere formation assay and soft-agar colony formation assay, while the expression of uPAR was analyzed by Western blot.
Results: Compared with NCI-H446 cells, the sphere formation rate, colony formation rate, and the expression of MnSOD and uPAR were significantly increased in the second passage sphere formation cells in NCI-H446 cells (P<0.05). Silence of MnSOD inhibited the sphere formation rate, colony formation rate, and the expression level of uPAR in the second passage sphere formation cells in NCI-H446 cells.
Conclusion: MnSOD may promote tumorigenicity in NCI-H446 cells by up-regulation of uPAR expression in vitro.