Evidence map›Paper›PMID 34109431›Full record

ArticleMolecular medicine reports2021

miR‑200b upregulation promotes migration of BEAS‑2B cells following long‑term exposure to cigarette smoke by targeting ETS1.

Jin Wang, Ruixin Yao, Qiulin Luo, Lirong Tan, Beibei Jia, Nan Ouyang, Yezhou Li, Jian Tong, Jianxiang Li

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.3field-weighted citation impact, top 50% 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

1 citing paper in PubMed, 5 citations in OpenAlex.

  1. Article
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

9 authors at 2 institutions in 2 countries.

Jin WangDepartment of Toxicology, School of Public Health, Medical College of Soochow University, Suzhou, Jiangsu 215123, P.R. China.
Ruixin YaoDepartment of Toxicology, School of Public Health, Medical College of Soochow University, Suzhou, Jiangsu 215123, P.R. China.
Qiulin LuoDepartment of Toxicology, School of Public Health, Medical College of Soochow University, Suzhou, Jiangsu 215123, P.R. China.
Lirong TanDepartment of Toxicology, School of Public Health, Medical College of Soochow University, Suzhou, Jiangsu 215123, P.R. China.
Beibei JiaDepartment of Toxicology, School of Public Health, Medical College of Soochow University, Suzhou, Jiangsu 215123, P.R. China.
Nan OuyangDepartment of Toxicology, School of Public Health, Medical College of Soochow University, Suzhou, Jiangsu 215123, P.R. China.
Yezhou LiSchool of Medicine, University of Manchester, M13 9PL Manchester, UK.
Jian TongDepartment of Toxicology, School of Public Health, Medical College of Soochow University, Suzhou, Jiangsu 215123, P.R. China.
Jianxiang LiDepartment of Toxicology, School of Public Health, Medical College of Soochow University, Suzhou, Jiangsu 215123, P.R. China.
Soochow University · CNUniversity of Manchester · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cigarette smoking is the leading cause of all histological types of lung cancer, and the role that microRNAs (miRNAs) serve in its pathogenesis is being increasingly recognized. The aim of the present study was to investigate the role of miR‑200b on migration in cigarette smoke‑induced malignant transformed cells. In the present study, miR‑200b expression was found to be increased in cigarette smoke (CS)‑exposed BEAS‑2B cells, lung cancer cell lines and tumor tissue samples. Using wound healing and Transwell migration assays, the migratory ability was shown to be increased in miR‑200b‑overexpressing cells, whereas miR‑200b knockdown resulted in reduced migration. Additionally, the expression of E‑Cadherin was downregulated, whereas that of N‑Cadherin was upregulated in miR‑200b mimic‑transfected cells, suggesting an increase in epithelial‑mesenchymal transition. Downstream, using four target gene prediction tools, six target genes of miR‑200b were predicted, amongst which, ETS proto‑oncogene 1 transcription factor (

Indexed as

Gene Expression Regulation, NeoplasticAdenocarcinoma of LungAntigens, CDCadherinsCarcinoma, Squamous CellCell LineCell MovementEpithelial CellsEpithelial-Mesenchymal TransitionHumansLung NeoplasmsMicroRNAsNicotianaProto-Oncogene Protein c-ets-1SmokingTime FactorsAntigens, CDCadherinsCDH1 protein, humanCDH2 protein, humanETS1 protein, humanMicroRNAsMIRN200 microRNA, humanProto-Oncogene Protein c-ets-1cigarette smokelung cancermicroRNA‑200bmigration

Identifiers

PMID34109431
PMCPMC8201442
OpenAlexW3165994359

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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Registered trials

None linked

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.