Journal
CANCER SCIENCE
Volume 100, Issue 5, Pages 807-812Publisher
WILEY
DOI: 10.1111/j.1349-7006.2009.01121.x
Keywords
-
Categories
Funding
- Ministry of Education, Culture, Sports, Science and Technology of Japan [19591122]
- Takeda Science Foundation
- Japan Leukemia Research Fund
- Princes Takamatsu Cancer Research Fund [07-23905]
- Kanehara Ichiro Memorial Foundation for Promotion of Medicine
- Grants-in-Aid for Scientific Research [19591122] Funding Source: KAKEN
Ask authors/readers for more resources
The Epstein-Barr virus-encoded latent membrane protein 1 is considered the Epstein-Barr virus oncogene based on its importance in Epstein-Barr virus-induced B-lymphocyte transformation. beta-Catenin is a potential oncogene, and its accumulation has been implicated in a variety of human cancers. Here, we found that beta-catenin protein was highly expressed in Epstein-Barr virus-immortalized B-cell lines compared with peripheral blood mononuclear cells from healthy donors. beta-Catenin expression in Epstein-Barr virus-immortalized B-cell line decreased following treatment with LY294002, an inhibitor of phosphatidylinositol 3-kinase. Treatment with LY294002 or knockdown of beta-catenin by small interfering RNA reduced the growth of Epstein-Barr virus-immortalized B-cell line. Transient transfection of latent membrane protein 1 expression plasmid increased beta-catenin protein expression and beta-catenin-dependent transcription. Latent membrane protein 1 deletions mutants lacking the carboxyl-terminal activating region 1 domain failed to enhance beta-catenin protein expression and beta-catenin-dependent transcriptional activity. They also failed to increase phosphorylated AKT expression. Dominant-negative AKT suppressed latent membrane protein 1-induced beta-catenin-dependent transcriptional activity. These results suggest that latent membrane protein 1 activates beta-catenin through the phosphatidylinositol 3-kinase/AKT signaling pathway. Activation of the beta-catenin pathway by Epstein-Barr virus may contribute to the lymphoproliferation characteristic of Epstein-Barr virus-infected B-cells. (Cancer Sci 2009; 100: 807-812).
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