癌症研究
细胞生长
小发夹RNA
肿瘤进展
抑制器
细胞凋亡
肺癌
细胞迁移
生物
癌症
基因沉默
医学
细胞
内科学
基因敲除
遗传学
基因
生物化学
作者
Yan Li,Fen Zhao,Ping Zhang,Peng Duan,Yangmei Shen
出处
期刊:Human Cell
[Springer Nature]
日期:2019-12-07
卷期号:33 (1): 220-231
被引量:13
标识
DOI:10.1007/s13577-019-00305-w
摘要
Non-small cell lung cancer (NSCLC) is a malignant tumor with a high fatality, low overall cure, and survival rates worldwide. When only palliative therapy is available, the disease leads to malignant proliferation. Previous studies showed miR-29b serves as an NSCLC suppressor by inhibiting cells proliferation, migration, and invasion. However, the mechanism underlying NSCLC progression remains elusive. In this study, we identified Striatin 4 (STRN4), a target of miR-29b, which serves as a pro-oncogenic protein by promoting cells proliferation, migration, and invasion in NSCLC. Besides, the STRN4 was highly expressed in NSCLC and negatively regulated by miR-29b. Down-regulation of STRN4 inhibits NSCLC cells proliferation, migration, invasion, and promotes apoptosis in vitro, whereas overexpression-induced enhanced cell migration and invasion could be reverved by miR-29b. Notably, overexpression of miR-29b and down-regulation of STRN4 by shRNA suppressed cellular proliferation and delayed tumor progression in vivo. Together, these findings identify a miR-29b/STRN4 regulatory pathway in NSCLC progression, which may provide a new sight for the treatment of NSCLC.
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