当前位置: 首页 > 详情页

AdipoR1-mediated miR-3908 inhibits glioblastoma tumorigenicity through downregulation of STAT2 associated with the AMPK/SIRT1 pathway

文献详情

资源类型:

收录情况: ◇ SCIE

机构: [1]Department of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, Beijing 100050 [2]Department of Oncology, Beijing Ditan Hospital, Capital Medical University, Beijing 100015 [3]Department of Laboratory Medicine, the Second People's Hospital of Guangdong Province, Southern Medical University, Guangzhou, Guangdong 510317 [4]Department of Laboratory Medicine, the Affiliated Hospital of Medical College of Qingdao University, Qingdao, Shandong 266000, P.R. China
出处:
ISSN:

关键词: microRNA STAT2 AMPK SIRT1 glioblastoma tumorigenicity

摘要:
A prospective method of treatment for cancer is to inhibit oncogene signaling pathways with microRNA (miRNA or miR). In the present study, whether the expression of STAT2, AdipoR1/AMPK/SIRT1 pathway of glioma is regulated by miR-3908 was explored. To confirm whether the predicted miR-3908 is matched with STAT2 and AdipoR1, 3'UTR luciferase activity of STAT2 and AdipoRl was assessed. In the presence of the mimics or inhibitors of miR-3908, cell function of glioma cells, such as proliferation, growth, migration, invasion and apoptosis were analyzed. The expression of AdipoRl and its downstream AMPK/SIRT1 pathway proteins or STAT2 were examined. Luciferase reporter analysis showed that miR-3908 directly target STAT2 and AdipoRl. miR-3908 suppressed expression of STAT2 or AdipoRl and downregulated AdipoRl pathway genes, including AMPK, p-AMPK and SIRT1. miR-3908 inhibited tumorigenicity, migration, growth and invasion in glioma cell lines U251 and U87 as well as increased apoptosis of these cells. The pathways related to tumorigenicity and tumor progression, STAT2 and AdipoR1/AMPK/SIRT1 could be restrained by miR-3908. In conclusion, restoration of miR-3908 expression induced suppression of cancer progression and glioblastoma tumorigenicity. The present study discovered novel tumorigenesis associated with miR-3908, which may represent a new target in treatment for glioblastoma.

基金:
语种:
被引次数:
WOS:
PubmedID:
中科院(CAS)分区:
出版当年[2016]版:
大类 | 3 区 医学
小类 | 4 区 肿瘤学
最新[2023]版:
大类 | 3 区 医学
小类 | 4 区 肿瘤学
JCR分区:
出版当年[2015]版:
Q3 ONCOLOGY
最新[2023]版:
Q2 ONCOLOGY

影响因子: 最新[2023版] 最新五年平均 出版当年[2015版] 出版当年五年平均 出版前一年[2014版] 出版后一年[2016版]

第一作者:
第一作者机构: [1]Department of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, Beijing 100050
通讯作者:
通讯机构: [2]Department of Oncology, Beijing Ditan Hospital, Capital Medical University, Beijing 100015 [3]Department of Laboratory Medicine, the Second People's Hospital of Guangdong Province, Southern Medical University, Guangzhou, Guangdong 510317 [4]Department of Laboratory Medicine, the Affiliated Hospital of Medical College of Qingdao University, Qingdao, Shandong 266000, P.R. China [*1]Department of Laboratory Medicine, the Second People's Hospital of Guangdong Province, Southern Medical University, No. 466 Xingangzhong road, Haizhu, Guangzhou, Guangdong 510317, P.R. China [*2]Department of Oncology, Beijing Ditan Hospital, Capital Medical University, No. 8 Jingshun East Street, Chaoyang, Beijing 100015, P.R. China
推荐引用方式(GB/T 7714):
APA:
MLA:

资源点击量:16470 今日访问量:0 总访问量:871 更新日期:2025-01-01 建议使用谷歌、火狐浏览器 常见问题

版权所有©2020 首都医科大学宣武医院 技术支持:重庆聚合科技有限公司 地址:北京市西城区长椿街45号宣武医院