4.5 Article Retracted Publication

被撤回的出版物: Epstein-Barr virus-encoded latent membrane protein 1 activates β-catenin signaling in B lymphocytes (Retracted article. See vol. 102, pg. 500, 2011)

期刊

CANCER SCIENCE
卷 100, 期 5, 页码 807-812

出版社

WILEY
DOI: 10.1111/j.1349-7006.2009.01121.x

关键词

-

类别

资金

  1. Ministry of Education, Culture, Sports, Science and Technology of Japan [19591122]
  2. Takeda Science Foundation
  3. Japan Leukemia Research Fund
  4. Princes Takamatsu Cancer Research Fund [07-23905]
  5. Kanehara Ichiro Memorial Foundation for Promotion of Medicine
  6. Grants-in-Aid for Scientific Research [19591122] Funding Source: KAKEN

向作者/读者索取更多资源

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).

作者

我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。

评论

主要评分

4.5
评分不足

次要评分

新颖性
-
重要性
-
科学严谨性
-
评价这篇论文

推荐

暂无数据
暂无数据