Journal
ONCOTARGET
Volume 7, Issue 24, Pages 37000-37012Publisher
IMPACT JOURNALS LLC
DOI: 10.18632/oncotarget.9454
Keywords
glutaredoxin 3; nasopharyngeal carcinoma; EGFR; Akt
Categories
Funding
- National Natural Scientific Foundation of China [81272983]
- Guangxi Key Laboratory of Early Prevention in Regional High Incidence Cancer [GKE2015-ZZ07]
- Guangxi Natural Science Foundation [2013GXNSFGA 019002]
Ask authors/readers for more resources
Glutaredoxin 3 (GLRX3) is antioxidant enzyme, maintaining a low level of ROS, thus contributing to the survival and metastasis of several types of cancer. However, the expression and functions of GLRX3 have not been addressed in nasopharyngeal carcinoma (NPC). In this study, we found that GLRX3 was overexpressed in NPC. Knockdown of GLRX3 in NPC cell lines inhibited proliferation in vitro, tumorignesis in vivo, and colony formation. In addition, GLRX3 knockdown decreased the migration and invasion capacity of NPC cells by reversing the epithelial-mesenchymal transition (EMT). Furthermore, stabilization of GLRX3 was positively related to with epidermal growth factor receptor (EGFR) expression and negatively with ROS generation. Phosphorylation of Akt, a key downstream effector, was induced by EGFR signaling but did not rely on increasing ROS level in NPC cells. GLRX3 might be an oncoprotein in NPC, playing important roles in increasing redox reaction and activating EGFR/Akt signals, so it may be a therapeutic target for NPC.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available