Suppression of Epithelial Mesenchymal Transition and Metastasis in Nasopharyngeal Carcinoma via SOD1 Inhibition
- VernacularTitle:抑制SOD1调节上皮间质转化抑制鼻咽癌细胞迁移
- Author:
Lanyan FU
;
Liwen DENG
;
Ting DAI
;
Liling JIANG
;
Qing GONG
;
Shuai LI
- Keywords:
epithelial-mesenchymal transition;
nasopharyngeal carcinoma;
superoxide dismutase 1
- From:
Journal of Sun Yat-sen University(Medical Sciences)
2017;38(1):42-48
- CountryChina
- Language:Chinese
-
Abstract:
Objective]To explore the aberrant expression of SOD1 gene in nasopharyngeal carcinoma tissues and adjacent tissues,as well as in NPC cell lines,then to observe the effect of SOD1 on NPC cells metastatic ability and investigate the intrinsic?mechanism.[Methods]Immunohistochemical technique was used to examine SOD1 expression in carcinoma tissues and adjacent tissues(n=10). Small interfering RNAs and inhibitor LCS-1 were used to knockdown of SOD1 expression and inhibit SOD1 activity, respectively. Then,wound healing test and migration assay were applied to detect cell metastatic ability in vitro. Real-time PCR and Western Blot were used to analyze the expression of EMT-related genes(E-cadherin,Vimentin,Twist).[Results]SOD1 was found to be significantly up-regulated in nasopharyngeal carcinoma tissues(n = 7 ,70%),compared to control. SOD1 was also highly expressed in highly metastatic potential NPC cell lines(CNE2,5-8F,S18)compared with low metastatic ability cell lines(6-10B). Knockdown SOD1 expression or inhibit SOD1 activity suppress cell motility in CNE2 and 5-8F cells. Finally,we demonstrate that SOD1 inhibition plays a role in induction of epithelial marker E-cadherin and has an opposite effect on mesenchymal marker vimen tin and transcriptional factor twist.[Conclusion]These results suggest that SOD1 contributes to EMT and might be important for tumor metastasis in NPC.
