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长链非编码 RNA SNHG5 通过 miR-132/PTEN 轴调控 COPD 细胞凋亡和炎症。

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

机构信息

Department of Respiratory Medicine, Hunan Provincial People's Hospital (The First Affiliated Hospital of Hunan Normal University), Changsha 410005, China.

Scientific Research Department, Hunan Provincial People's Hospital (The First Affiliated Hospital of Hunan Normal University), Changsha 410005, China.

出版信息

Biomed Pharmacother. 2020 Jun;126:110016. doi: 10.1016/j.biopha.2020.110016. Epub 2020 Mar 4.

Abstract

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.

摘要

长链非编码 RNA 小核仁 RNA 宿主基因 5(lncRNA SNHG5)在恶性进展中发挥明确的作用。然而,SNHG5 在慢性阻塞性肺疾病(COPD)进展中的作用尚不清楚。在本研究中,SNHG5 在 COPD 组织中低表达,并与患者的一秒用力呼气量(FEV1)%低呈正相关。随后,香烟烟雾提取物(CSE)降低了 16HBE 细胞中的 SNHG5 表达,而 16HBE 细胞中的 SNHG5 过表达减轻了 CSE 对增殖、凋亡和炎症(IL-1β、IL-6 和 TNF-a)的影响。在机制上,SNHG5 在 COPD 中作为 miR-132 的竞争性内源性 RNA(ceRNA)发挥作用,从而增加 miR-132 靶标 PTEN 的表达。此外,挽救实验表明,PTEN 抑制(或 miR-132 过表达)减弱了 SNHG5 上调对 COPD 进展的影响。总之,SNHG5-miR-132-PTEN 轴可能在 COPD 发病机制中发挥关键作用,为 COPD 的治疗提供了有效的靶点。

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