期刊
MOLECULAR THERAPY-NUCLEIC ACIDS
卷 14, 期 -, 页码 583-592出版社
CELL PRESS
DOI: 10.1016/j.omtn.2019.01.009
关键词
-
资金
- National Natural Science Foundation of China [NSFC 81572936, 81502126, 81773186]
- Natural Science Foundation of Bengbu Medical College [BYKY1770]
- program for graduate research of Bengbu Medical College [Byycxz1803]
Emerging evidence has demonstrated that miR-223 is critically involved in the progression of pancreatic cancer (PC); however, the underlying mechanisms are not fully elucidated. In the present study, we explored the molecular basis of miR-223-mediated tumor progression in PC. We performed numerous approaches including MTT, FACS, transfection, RT-PCR, western blotting, Transwell, and animal studies to determine the physiological role of miR-223 in PC cells. We found that sister chromatid cohesion protein PDS5 homolog B (PDS5B) is a direct target of miR-223 in PC. Moreover, PDS5B exhibits tumor-suppressive function in PC cells. Consistently, ectopic overexpression of PDS5B reversed miR-223-mediated tumor progression in PC cells. These results suggest that the miR-223/PDS5B axis regulates cell proliferation and invasion in PC cells. Our findings indicated that downregulation of miR-223 could be a novel therapeutic approach for PC.
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。
推荐
暂无数据