E2FBP1 antagonizes the p16INK4A-Rb tumor suppressor machinery for growth suppression and cellular senescence by regulating promyelocytic leukemia protein stability

Yayoi Fukuyo; Akiko Takahashi; Eiji Hara; Nobuo Horikoshi; Tej K.Pandita; Takuma Nakajima

首页> 外文期刊>国际口腔科学杂志（英文版） >E2FBP1 antagonizes the p16INK4A-Rb tumor suppressor machinery for growth suppression and cellular senescence by regulating promyelocytic leukemia protein stability

【24h】

E2FBP1 antagonizes the p16INK4A-Rb tumor suppressor machinery for growth suppression and cellular senescence by regulating promyelocytic leukemia protein stability

机译：E2FBP1通过调节早幼粒细胞白血病蛋白的稳定性来拮抗p16INK4A-Rb肿瘤抑制器的生长抑制和细胞衰老

获取原文

获取原文并翻译 | 示例

掌桥外文数据库（机构版） >>

开具论文收录证明 >>

文献代查 >>

页面导航

摘要
著录项
相关主题

摘要

Cellular senescence is an irreversible cell cycle arrest triggered by the activation of oncogenes or mitogenic signaling as well as the enforced expression of tumor suppressors such as p53, p16 INK4A and promyelocytic leukemia protein (PML) in normal cells. E2F-binding protein 1 (E2FBP1), a transcription regulator for E2F, induces PML reduction and suppresses the formation of PML-nuclear bodies, whereas the down-regulation of E2FBP1 provokes the PML-dependent premature senescence in human normal fibroblasts. Here we report that the depletion of E2FBP1 induces the accumulation of PML through the Ras-dependent activation of MAP kinase signaling. The cellular levels of p16 INK4A and p53 are elevated during premature senescence induced by depletion of E2FBP1, and the depletion of p16 INK4A , but not p53 rescued senescent cells from growth arrest. Therefore, the premature senescence induced by E2FBP1 depletion is achieved through the p16 INK4A -Rb pathway. Similar to human normal fibroblasts, the growth inhibition induced by E2FBP1 depletion is also observed in human tumor cells with intact p16 INK4A and Rb. These results suggest that E2FBP1 functions as a critical antagonist to the p16 INK4A -Rb tumor suppressor machinery by regulating PML stability.

著录项

来源
《国际口腔科学杂志（英文版）》 |2011年第4期|200-208|共9页
作者
Yayoi Fukuyo; Akiko Takahashi; Eiji Hara; Nobuo Horikoshi; Tej K.Pandita; Takuma Nakajima;
展开▼
作者单位

Department of Immunology,Tulane National Primate Research Center,Covington LA 70433,USA;

Section of Bacterial Pathogenesis,Graduate School,Tokyo Medical and Dental University,Tokyo 113-8549,Japan;

Division of Cancer Biology,The Cancer Institute,Japanese Foundation for Cancer Research,Tokyo 135-8550,Japan;

Division of Cancer Biology,The Cancer Institute,Japanese Foundation for Cancer Research,Tokyo 135-8550,Japan;

Division of Molecular Radiation Biology,Department of Radiation Oncology,University of Texas Southwestern Medical Center,Dallas TX 75390-8807,USA;

Division of Molecular Radiation Biology,Department of Radiation Oncology,University of Texas Southwestern Medical Center,Dallas TX 75390-8807,USA;

Section of Bacterial Pathogenesis,Graduate School,Tokyo Medical and Dental University,Tokyo 113-8549,Japan;

展开▼
收录信息中国科学引文数据库(CSCD);
原文格式 PDF
正文语种 chi
中图分类
关键词

E2FBP1 antagonizes the p16INK4A-Rb tumor suppressor machinery for growth suppression and cellular senescence by regulating promyelocytic leukemia protein stability

摘要

著录项

相关主题

期刊订阅