MiR-663 inhibits radiation-induced bystander effects by targeting TGFB1 in a feedback mode
文献类型：期刊论文
| 作者 | Hei, Tom K.1; Hong, Mei4; Wu, Xin2,3; Pei, Hailong2,3; Chang, Lei2; Ding, Nan2,3 ; Gao, Xiaofei2; Ye, Caiyong2,3; Wang, Jufang2; Zhou, Guangming2
|
| 刊名 | RNA BIOLOGY
 |
| 出版日期 | 2014-09-01 |
| 卷号 | 11页码:1189-1198 |
| ISSN号 | 1547-6286 |
| 关键词 | Microrna Tgf-1 Mir-663 Bystander Effects Ionizing Radiation |
| DOI | 10.4161/rna.34345 |
| 文献子类 | Article |
| 英文摘要 | The mechanisms of radiation-induced bystander effects (RIBE) have been investigated intensively over the past two decades. Although quite a few reports demonstrated that cytokines such as TGF-1 are induced within the directly irradiated cells and play critical roles in mediating the bystander effects, little is known about the signaling pathways that occur in bystander cells. The crucial question as to why RIBE signals cannot be infinitely transmitted, therefore, remains unclear. In the present study, we showed that miR-663, a radiosensitive microRNA, participates in the regulation of biological effects in both directly irradiated and bystander cells via its targeting of TGF-1. MiR-663 was downregulated, while TGFB1 was upregulated in directly irradiated cells. The regulation profile of miR-663 and TGFB1, on the other hand, was reversed in bystander cells, in which an elevated miR-663 expression was exhibited and led to downregulation of TGF-1. Further studies revealed that miR-663 interacts with TGFB1 directly and that through its binding to the core regulation sequence, miR-663 suppresses the expression of TGFB1. Based on the results, we propose that miR-663 inhibits the propagation of RIBE in a feedback mode, in which the induction of TGF-1 by reduced miR-663 in directly irradiated cells leads to increased level of miR-663 in bystander cells. The upregulation of miR-663 in turn suppresses the expression of TGF-1 and limits further transmission of the bystander signals. |
| WOS关键词 | GROWTH-FACTOR-BETA ; TRANSFORMING GROWTH-FACTOR-BETA-1 ; ALPHA-PARTICLES ; GLIOMA-CELLS ; SIGNALING PATHWAY ; MESSENGER-RNA ; NITRIC-OXIDE ; RAT-HEART ; IN-SITU ; DAMAGE |
| 资助项目 | US. National Institutes of Health[P01 CA 049062-21] |
| WOS研究方向 | Biochemistry & Molecular Biology |
| 语种 | 英语 |
| 出版者 | LANDES BIOSCIENCE |
| WOS记录号 | WOS:000348463500011 |
| 源URL | [http://119.78.100.186/handle/113462/49581]  |
| 专题 | 近代物理研究所_生物物理研究室 |
| 通讯作者 | Zhou, Guangming |
| 作者单位 | 1.Columbia Univ, Ctr Radiol Res, Med Ctr, New York, NY 10032 USA 2.Chinese Acad Sci, Inst Modern Phys, Key Lab Heavy Ion Radiat Biol & Med, Dept Space Radiobiol, Lanzhou, Peoples R China 3.Univ Chinese Acad Sci, Beijing, Peoples R China 4.South China Agr Univ, Coll Life Sci, Guangzhou, Guangdong, Peoples R China |
| 推荐引用方式 GB/T 7714 | Hei, Tom K.,Hong, Mei,Wu, Xin,et al. MiR-663 inhibits radiation-induced bystander effects by targeting TGFB1 in a feedback mode[J]. RNA BIOLOGY,2014,11:1189-1198. |
| APA | Hei, Tom K..,Hong, Mei.,Wu, Xin.,Pei, Hailong.,Chang, Lei.,...&Yao, Bin.(2014).MiR-663 inhibits radiation-induced bystander effects by targeting TGFB1 in a feedback mode.RNA BIOLOGY,11,1189-1198. |
| MLA | Hei, Tom K.,et al."MiR-663 inhibits radiation-induced bystander effects by targeting TGFB1 in a feedback mode".RNA BIOLOGY 11(2014):1189-1198. |
入库方式： OAI收割
来源：近代物理研究所
浏览0
下载0
收藏0
其他版本
除非特别说明，本系统中所有内容都受版权保护，并保留所有权利。