Evidence map›Paper›PMID 34266334›Full record

ArticleTherapeutic advances in respiratory disease

LncRNA CASC2 is involved in the development of chronic obstructive pulmonary disease

Panpan Liu, Huali Zhang, Haizhu Zeng, Yingxia Meng, Hongchang Gao, Meilan Zhang, Lei Zhao

Open access · goldAbstract read
In one paragraph

Article in Therapeutic advances in respiratory disease. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
1.3field-weighted citation impact, top 22% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.

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  10. Roles of noncoding RNAs in chronic obstructive pulmonary disease.Journal of translational internal medicine · 2023
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Panpan LiuDepartment of Pulmonary and Critical Care Medicine, Shanghai Pudong New Area Gongli Hospital, Shanghai, PR China.
Huali ZhangDepartment of Pulmonary and Critical Care Medicine, Shanghai Pudong New Area Gongli Hospital, Shanghai, PR China.
Haizhu ZengDepartment of Pulmonary and Critical Care Medicine, Shanghai Pudong New Area Gongli Hospital, Shanghai, PR China.
Yingxia MengDepartment of Pulmonary and Critical Care Medicine, Shanghai Pudong New Area Gongli Hospital, Shanghai, PR China.
Hongchang GaoDepartment of Pulmonary and Critical Care Medicine, Shanghai Pudong New Area Gongli Hospital, Shanghai, PR China.
Meilan ZhangDepartment of Pulmonary and Critical Care Medicine, Shanghai Pudong New Area Gongli Hospital, Shanghai, PR China.
Lei ZhaoDepartment of Pulmonary and Critical Care Medicine, Shanghai Pudong New Area Gongli Hospital, 219 Miao-Pu Road, Shanghai 200315, PR China.ORCID 0000-0002-2861-9265
Second Military Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsChronic 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.

methodsFifty 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.

resultsSerum 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.

conclusionCASC2 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

Indexed as

Pulmonary Disease, Chronic ObstructiveRNA, Long NoncodingTumor Suppressor ProteinsHumansInflammationInsulin-Like Growth Factor IMicroRNAsInsulin-Like Growth Factor Ilong non-coding RNA CASC2, humanMicroRNAsMIRN18A microRNA, humanRNA, Long NoncodingTumor Suppressor Proteinsbronchial epithelial cell apoptosisCASC2diagnosisinflammatorymiR-18a-5p

Identifiers

PMID34266334
PMCPMC8290508
OpenAlexW3180150730

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.