Evidence map›Paper›PMID 29118928›Full record

ArticleAmerican journal of translational research2017

MiR-5100 targets TOB2 to drive epithelial-mesenchymal transition associated with activating smad2/3 in lung epithelial cells.

Chun-Yan Li, Ya-Hong Wang, Zi-Ying Lin, La-Wei Yang, Sheng-Lan Gao, Tie Liu, Bao-An Zou, Zhan-Chun Pan, Ze-Qing Song, Gang Liu

Open access · greenAbstract read
In one paragraph

Article in American journal of translational research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.4field-weighted citation impact, top 42% 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

12 citing papers in PubMed, 11 citations in OpenAlex.

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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

10 authors at 2 institutions in 1 country.

Chun-Yan LiDepartment of Respiratory Medicine, Affiliated Hospital of Guangdong Medical UniversityZhanjiang 524001, China.
Ya-Hong WangClinical Research Center, Affiliated Hospital of Guangdong Medical UniversityZhanjiang 524001, China.
Zi-Ying LinClinical Research Center, Affiliated Hospital of Guangdong Medical UniversityZhanjiang 524001, China.
La-Wei YangClinical Research Center, Affiliated Hospital of Guangdong Medical UniversityZhanjiang 524001, China.
Sheng-Lan GaoClinical Research Center, Affiliated Hospital of Guangdong Medical UniversityZhanjiang 524001, China.
Tie LiuImmunology and Tumor Research Instituted, The First Affiliate Hospital, Xi'an Jiaotong University Health Science CenterXi'an 710061, Shaanxi, China.
Bao-An ZouDepartment of Respiratory Medicine, Affiliated Hospital of Guangdong Medical UniversityZhanjiang 524001, China.
Zhan-Chun PanDepartment of Respiratory Medicine, Affiliated Hospital of Guangdong Medical UniversityZhanjiang 524001, China.
Ze-Qing SongDepartment of Respiratory Medicine, Affiliated Hospital of Guangdong Medical UniversityZhanjiang 524001, China.
Gang LiuClinical Research Center, Affiliated Hospital of Guangdong Medical UniversityZhanjiang 524001, China.
Guangdong Medical College · CNFirst Affiliated Hospital of Xi'an Jiaotong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Idiopathic pulmonary fibrosis (IPF) is a devastating disease and the pathogenesis of IPF remains unclear. Our previous study indicated that miR-5100 promotes the proliferation and metastasis of lung epithelial cells. In this study, we investigated the effect and mechanism of miR-5100 on bleomycin (BLM)-induced mouse lung fibrosis and transforming growth factor β (TGF-β1) or epidermal growth factor (EGF) induced EMT-model in A549 and Beas-2B cells. The elevated level of miR-5100 was observed in both the mouse lung fibrosis tissues and EMT cell model. Furthermore, the exogenous expression of miR-5100 promoted the EMT-related changes, enhanced TGF-β1 or EGF-induced EMT and activated the smad2/3 in lung epithelial cells, while silencing miR-5100 had the converse effects. In addition, transwell assay showed that miR-5100 can enhance cell migration. Using target prediction software and luciferase reporter assays, we identified TOB2 as a specific target of miR-5100 and miR-5100 can decrease the accumulation of endogenous TOB2 in A549 and Beas-2B cells. Moreover, the exogenous expression of TOB2 relieves the promotion of miR-5100 on EMT process and migration ability. Taken together, our results indicate that miR-5100 promotes the EMT process by targeting TOB2 associated with activating smad2/3 in lung epithlium cells. Our findings may provide novel insights into the pathogenesis of IPF.

Indexed as

epithelial-mesenchymal transition (EMT)idiopathic pulmonary fibrosis (IPF)lung epithelial cellmiR-5100smad2/3TOB2

Identifiers

PMID29118928
PMCPMC5666075
OpenAlexW2947020280

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.