慢性阻塞性肺病
PTEN公司
下调和上调
竞争性内源性RNA
炎症
小RNA
癌症研究
细胞凋亡
医学
生物
长非编码RNA
免疫学
内科学
基因
PI3K/AKT/mTOR通路
遗传学
作者
Qin Shen,Jiao Zheng,Xueling Wang,Wen Hu,Yan Jiang,Yong-Liang Jiang
标识
DOI:10.1016/j.biopha.2020.110016
摘要
Long non-coding RNAs small nucleolar RNA host gene 5 (lncRNA SNHG5) plays well-defined roles in the malignant progression. However, the roles of SNHG5 in chronic obstructive pulmonary disease (COPD) progression remain unclear. In the present study, SNHG5 expression was low expressed in COPD tissues and positively correlated with low forced expiratory volume in one second (FEV1)% in patients. Subsequently, cigarette smoke extract (CSE) decreased SNHG5 expression in 16HBE cells, and SNHG5 overexpression in 16HBE cells mitigated the effects of CSE on the proliferation, apoptosis and inflammation (IL-1β, IL-6 and TNF-a). Mechanistically, SNHG5 functioned as a competing endogenous RNA (ceRNA) for miR-132 in COPD, thereby increasing the expression of the miR-132 target PTEN. Moreover, rescue assays demonstrated that PTEN suppression (or miR-132 overexpression) attenuated the effects of SNHG5 upregulation on COPD progression. In conclusion, the SNHG5-miR-132-PTEN axis might play critical roles in COPD development, providing an effective target for the treatment of COPD.
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