Evidence map›Paper›PMID 34295155›Full record

ArticleInternational journal of chronic obstructive pulmonary disease2021

Circ-RBMS1 Knockdown Alleviates CSE-Induced Apoptosis, Inflammation and Oxidative Stress via Up-Regulating FBXO11 Through miR-197-3p in 16HBE Cells.

Di Qiao, Chi Hu, Qiuyan Li, Jun Fan

Open access · goldAbstract read
In one paragraph

Article in International journal of chronic obstructive pulmonary disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

16 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
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  9. Circular RNAs: emerging players in asthma and COPD.Frontiers in cell and developmental biology · 2023
    Review
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  11. Article
  12. Review
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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

4 authors at 2 institutions in 1 country.

Di QiaoDepartment of Respiratory Medicine, Kunming Tongren Hospital, Kunming City, Yunnan Province, People's Republic of China.
Chi HuDepartment of Respiratory Medicine, Kunming Tongren Hospital, Kunming City, Yunnan Province, People's Republic of China.
Qiuyan LiDepartment of Respiratory Medicine, Kunming Tongren Hospital, Kunming City, Yunnan Province, People's Republic of China.
Jun FanDepartment of Cardiovascular Medicine, Chinese People's Liberation Army Joint Service Support Unit 920 Hospital, Kunming City, Yunnan Province, People's Republic of China.
Kunming Tongren Hospital · CNChinese People's Liberation Army · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Emerging evidence has reported that circular RNAs (circRNAs) are aberrantly expressed and act as significant regulators in pathological processes of chronic obstructive pulmonary disease (COPD). Here, the purpose of this article was to evaluate and clarify the biological functions and mechanism of circRNA single stranded interacting protein 1 (circ-RBMS1) in cigarette smoke (CS)-induced COPD. Methods: Human bronchial epithelial cells 16HBE treated with or without cigarette smoke extract (CSE) were used in the experimental group in vitro. Levels of circ-RBMS1, microRNA (miR)-197-3p, and F-box only protein 11 (FBXO11) were detected using quantitative real-time polymerase chain reaction and Western blot. The present study used cell counting kit-8 (CCK-8), 5-ethynyl-2'-deoxyuridine (EDU), flow cytometry and Western blot assays to determine the survival of 16HBE cells. The activity of interleukin (IL)-1β, tumor necrosis factor (TNF-α), malondialdehyde (MDA) and superoxide dismutase (SOD) was evaluated using the relative commercial kits. Dual-luciferase activity and RIP assays were used to identify the target relationship between miR-197-3p and circ-RBMS1 or FBXO11. Results: Circ-RBMS1 was highly expressed in COPD patients, and CSE induced an increased expression of circ-RBMS1 in a dose-dependent manner. Functionally, knockdown of circ-RBMS1 attenuated CSE-induced apoptosis, inflammation and oxidative stress in 16HBE cells. Circ-RBMS1 directly targeted miR-197-3p, and miR-197-3p inhibition reversed the effects of circ-RBMS1 knockdown on CSE-induced 16HBE cells. FBXO11 was a target of miR-197-3p. MiR-197-3p overexpression or FBXO11 silencing reduced the apoptosis, inflammation and oxidative stress in CSE-induced 16HBE cells. Moreover, miR-197-3p exerted its effects by targeting FBXO11. Additionally, circ-RBMS1 acted as a sponge for miR-197-3p to positively regulate FBXO11 expression in 16HBE cells. Conclusion: Circ-RBMS1 knockdown alleviated CSE-induced apoptosis, inflammation and oxidative stress in 16HBE cells via miR-197-3p/FBXO11 axis, suggesting a new insight into the pathogenesis of CS-induced COPD.

Indexed as

F-Box ProteinsMicroRNAsPulmonary Disease, Chronic ObstructiveApoptosisDNA-Binding ProteinsGene Knockdown TechniquesHumansInflammationOxidative StressProtein-Arginine N-MethyltransferasesRNA-Binding ProteinsRNA, CircularDNA-Binding ProteinsF-Box ProteinsFBXO11 protein, humanMicroRNAsMIRN197 microRNA, humanProtein-Arginine N-MethyltransferasesRBMS1 protein, humanRNA-Binding ProteinsRNA, Circularapoptosiscirc-RBMS1COPDFBXO11inflammationmiR-197-3p

Identifiers

PMID34295155
PMCPMC8291609
OpenAlexW3178753798

What OpenQuestion holds

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LicenceCC BY-NC
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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.