Role of long non‑coding RNA MALAT1 in chronic obstructive pulmonary disease
- Tian‑Jun Hu
- Hong‑Bo Huang
- Hai‑Bo Shen
- Wei Chen
- Zhen‑Hua Yang
Affiliations: Department of Thoracic Surgery, Hwa Mei Hospital, University of Chinese Academy of Sciences, Ningbo, Zhejiang 315012, P.R. China, Zhongyuan Union Clinical Laboratory Co. Ltd., Tianjin 300384, P.R. China
- Published online on: July 13, 2020 https://doi.org/10.3892/etm.2020.8996
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et al. This is an open access article distributed under the
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Chronic obstructive pulmonary disease (COPD) is a pathological inflammatory condition of the lungs that is associated with high rates of mortality. Although long non‑coding RNAs (lncRNAs) serve a role in lung diseases, their functions in COPD pathogenesis are relatively unknown. The present study aimed to assess the role of differentially expressed lncRNAs in COPD. Expression profile analysis of six lncRNAs in age‑matched COPD and non‑COPD tissues were conducted. Among the six tested lncRNAs, metastasis‑associated in lung adenocarcinoma transcript 1 (MALAT1) was the most consistently overexpressed in COPD lung tissue specimens. To model COPD in vitro, human lung fibroblasts were treated with transforming growth factor‑β (TGF‑β) and MALAT1 was knocked down by small interfering RNA. This promoted cell viability and concurrently inhibited the expression of mesenchymal proteins, fibronectin and α‑smooth muscle actin. In COPD, cell senescence is linked to the activation of mammalian target of rapamycin complex 1 (mTORC1). Upon gene silencing of MALAT1 in non‑TGF‑β‑treated cells, cells demonstrated constitutive activation of mTORC1, which was assessed by the protein expression levels of mTORC1 substrate S6 kinase (S6K1). By contrast, upon MALAT1 silencing in the TGF‑β‑treated cells, mTORC1 activation was not suppressed, despite the mesenchymal cell markers protein expression levels being downregulated. Thus, lncRNA MALAT1 may represent a potent biomarker in COPD patients and may act as a target for both diagnostic and therapeutic purposes.