Journal
INTERNATIONAL JOURNAL OF ONCOLOGY
Volume 48, Issue 2, Pages 756-764Publisher
SPANDIDOS PUBL LTD
DOI: 10.3892/ijo.2015.3297
Keywords
TP53-induced glycolysis and apoptosis regulator; nasopharyngeal carcinoma; xenograft model; NF-kappa B pathway
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Funding
- National Natural Science Foundation [81201784]
- Scientific Research Foundation of the Education Department of Sichuan Province [15ZA0163]
- Union Project of Luzhou City and Sichuan Medical University [2013LZLY-J40]
- First Hospital of Sichuan Medical University Foundation [201519]
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The TP53-induced glycolysis and apoptosis regulator (TIGAR) is a p53 target gene, which functions to suppress reactive oxygen species (ROS) damage and protect cells from apoptosis. In this study, we investigated the role of TIGAR in nasopharyngeal carcinoma (NPC) tumorigenesis. Imnunohistochemical analysis of the tissue specimens from nasopharyngeal carcinoma patients showed a higher expression level of TIGAR in tumor tissues, compared with normal nasopharyngeal epithelium. Knockdown of TIGAR by lentivirus-shRNA in CNE-2 or 5-8F cells resulted in decreased cell growth, colony formation, migration, invasion, and induced apoptosis. TIGAR overexpression exerted the opposite effects except for apoptosis reduction. In the xenograft tumor models, TIGAR knockdown reduced tumor growth rate and weight, whereas TIGAR overexpression showed the opposite effects. In addition, the NF-kappa B signaling pathway was decreased in TIGAR silenced cells. In conclusion, our data demonstrated that TIGAR acted as an oncogene in NPC tumorigenesis, and knockdown of TIGAR inhibited NPC tumor growth through the NF-kappa B pathway.
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