LncRNA SNHG5 regulates cell apoptosis and inflammation by miR-132/PTEN axis in COPD

• Published in: Biomedicine & pharmacotherapy 2020-06, Vol.126, p.110016-110016, Article 110016
• Main Authors: Shen, Qin, Zheng, Jiao, Wang, Xueling, Hu, Wen, Jiang, Yongjie, Jiang, Yongliang
• Format: Article
• Language: English
• Subjects: Apoptosis; Cell Line; Cell Proliferation; Chronic obstructive pulmonary disease; Down-Regulation; Gene Expression Regulation; Humans; Inflammation - metabolism; Long non-coding RNAs; MicroRNAs - genetics; MicroRNAs - metabolism; miR-132; PTEN; PTEN Phosphohydrolase - genetics; PTEN Phosphohydrolase - metabolism; Pulmonary Disease, Chronic Obstructive - metabolism; RNA, Long Noncoding - genetics; RNA, Long Noncoding - metabolism; SNHG5
• ISSN: 0753-3322; 1950-6007
• DOI: 10.1016/j.biopha.2020.110016

[Display omitted] •SNHG5 expression was low expressed in COPD.•CSE decreased SNHG5 expression.•The SNHG5-miR-132-PTEN axis in COPD. 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.