Targeting Epstein–Barr virus oncoprotein LMP1-mediated glycolysis sensitizes nasopharyngeal carcinoma to radiation therapy View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2014-09

AUTHORS

L Xiao, Z-Y Hu, X Dong, Z Tan, W Li, M Tang, L Chen, L Yang, Y Tao, Y Jiang, J Li, B Yi, B Li, S Fan, S You, X Deng, F Hu, L Feng, A M Bode, Z Dong, L-Q Sun, Y Cao

ABSTRACT

Our goal in this work was to illustrate the Epstein-Barr virus (EBV)-modulated global biochemical profile and provide a novel metabolism-related target to improve the therapeutic regimen of nasopharyngeal carcinoma (NPC). We used a metabolomics approach to investigate EBV-modulated metabolic changes, and found that the exogenous overexpression of the EBV-encoded latent membrane protein 1 (LMP1) significantly increased glycolysis. The deregulation of several glycolytic genes, including hexokinase 2 (HK2), was determined to be responsible for the reprogramming of LMP1-mediated glucose metabolism in NPC cells. The upregulation of HK2 elevated aerobic glycolysis and facilitated proliferation by blocking apoptosis. More importantly, HK2 was positively correlated with LMP1 in NPC biopsies, and high HK2 levels were significantly associated with poor overall survival of NPC patients following radiation therapy. Knockdown of HK2 effectively enhanced the sensitivity of LMP1-overexpressing NPC cells to irradiation. Finally, c-Myc was demonstrated to be required for LMP1-induced upregulation of HK2. The LMP1-mediated attenuation of the PI3-K/Akt-GSK3beta-FBW7 signaling axis resulted in the stabilization of c-Myc. These findings indicate a close relationship between EBV and glycolysis in NPC. Notably, LMP1 is the key regulator of the reprogramming of EBV-mediated glycolysis in NPC cells. Given the importance of EBV-mediated deregulation of glycolysis, anti-glycolytic therapy might represent a worthwhile avenue of exploration in the treatment of EBV-related cancers. More... »

PAGES

4568

References to SciGraph publications

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/onc.2014.32

DOI

http://dx.doi.org/10.1038/onc.2014.32

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1037683760

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/24662831


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457 1] Cancer Research Institute, Xiangya School of Medicine, Central South University, Changsha, China [2] Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Changsha, China [3] Key Laboratory of Carcinogenesis, Ministry of Health, Changsha, China [4] The First Hospital of Changsha City, Changsha, China.
458 1] Cancer Research Institute, Xiangya School of Medicine, Central South University, Changsha, China [2] Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Changsha, China [3] Key Laboratory of Carcinogenesis, Ministry of Health, Changsha, China.
459 rdf:type schema:Organization
 




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