Related Experiment Video
Updated: Oct 28, 2025
Overexpressing Long Noncoding RNAs Using Gene-activating CRISPR
Published on: March 1, 2019
LncRNA CASC2 is involved in the development of chronic obstructive pulmonary disease via targeting miR-18a-5p/IGF1
Panpan Liu1, Huali Zhang1, Haizhu Zeng1
1Department of Pulmonary and Critical Care Medicine, Shanghai Pudong New Area Gongli Hospital, Shanghai, PR China.
Aims:
Chronic obstructive pulmonary disease (COPD) is a systemic disease. Several long non-coding RNAs (lncRNAs) have been identified to be aberrantly expressed in COPD patients. This study investigated the role of lncRNA cancer susceptibility candidate 2 (CASC2) in COPD, as well as its potential mechanism.
Methods:
Fifty smokers with COPD and another 50 smokers without COPD were recruited. Receiver operating characteristic curve was constructed to assess the diagnostic value of CASC2 in COPD patients. 16HBE cells were treated with cigarette smoke extract (CSE) to establish a cell model. qRT-PCR was used for the measurement of mRNA levels. The cell viability and apoptosis were detected by using Cell Counting Kit-8 and flow cytometry assay. Enzyme-linked immunosorbent assay was performed to detect the levels of proinflammatory cytokines. Luciferase reporter assay was performed for the target gene analysis.
Results:
Serum CASC2 was dramatically decreased in COPD patients compared with smokers without COPD, and was positively associated with FEV1 (forced expiratory volume in one second). Serum CASC2 was overexpressed in severe COPD patients, and had the diagnostic accuracy to distinguish COPD patients from smokers. CASC2 overexpression alleviated CSE-induced apoptosis and inflammation in 16HBE cells. CASC2 functions as a ceRNA of miR-18a-5p. Upregulation of miR-18a-5p reversed the influence of CASC2 on cell apoptosis and inflammation in 16HBE cells. IGF1 was the target gene of miR-18a-5p.
Conclusion:
CASC2 was downregulated in COPD patients and it might be a promising biomarker for the disease diagnosis. Overexpression of CASC2 might inhibit the bronchial epithelial cell apoptosis and inflammation via targeting miR-18a-5p/IGF1 axis.The reviews of this paper are available via the supplemental material section.
Related Concept Videos
01:20Chronic Obstructive Pulmonary Disease-II: Pathophysiology
Chronic Inflammation
02:39lncRNA - Long Non-coding RNAs
02:39lncRNA - Long Non-coding RNAs
01:23Cystic Fibrosis: Pathogenesis
CF is primarily caused by a genetic mutation in a chromosome 7 gene coding for the cystic fibrosis transmembrane conductance regulator (CFTR) protein. The most common gene mutation leading to CF is the ΔF508 mutation,...
01:22Chronic Obstructive Pulmonary Disease
Smoking is a primary risk factor for COPD, with over 80% of patients having a history of it. Patients typically experience progressive dyspnea or labored breathing, frequent coughing, and recurrent pulmonary infections. Many eventually succumb to respiratory failure, characterized by...
01:20COPD: Pathogenesis and Clinical Features
The primary cause for the onset of COPD is cigarette smoking and exposure to air pollution. These hazardous factors initiate a chain reaction within the lungs, resulting in chronic inflammation, damage to the airways, and a...