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Glutaredoxin 3 promotes nasopharyngeal carcinoma growth and metastasis via EGFR/Akt pathway and independent of ROS.
- Source :
-
Oncotarget [Oncotarget] 2016 Jun 14; Vol. 7 (24), pp. 37000-37012. - Publication Year :
- 2016
-
Abstract
- 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.<br />Competing Interests: The authors declare no conflicts of interest.
- Subjects :
- Adult
Aged
Animals
Carcinoma metabolism
Cell Movement physiology
Epithelial-Mesenchymal Transition physiology
Female
Gene Expression Regulation, Neoplastic physiology
Heterografts
Humans
Male
Mice
Mice, Nude
Middle Aged
Nasopharyngeal Carcinoma
Nasopharyngeal Neoplasms metabolism
Neoplasm Invasiveness pathology
Reactive Oxygen Species
Signal Transduction physiology
Carcinoma pathology
Carrier Proteins metabolism
ErbB Receptors metabolism
Nasopharyngeal Neoplasms pathology
Proto-Oncogene Proteins c-akt metabolism
Subjects
Details
- Language :
- English
- ISSN :
- 1949-2553
- Volume :
- 7
- Issue :
- 24
- Database :
- MEDLINE
- Journal :
- Oncotarget
- Publication Type :
- Academic Journal
- Accession number :
- 27203742
- Full Text :
- https://doi.org/10.18632/oncotarget.9454