Evidence map›Paper›PMID 26647778›Full record

ArticleMolecular medicine reports2016

TGF-β2 induces epithelial-mesenchymal transition in cultured human lens epithelial cells through activation of the PI3K/Akt/mTOR signaling pathway.

Rui Guo, Qianli Meng, Haike Guo, Lijia Xiao, Xiaohong Yang, Ying Cui, Yu Huang

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.7field-weighted citation impact, top 7% 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, 38 citations in OpenAlex.

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  13. International journal of ophthalmology · 2018
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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 3 institutions in 1 country.

Rui GuoPostgraduate Institute, Southern Medical University, Guangzhou, Guangdong 510515, P.R. China.
Qianli MengDepartment of Ophthalmology, Guangdong Eye Institute, Guangdong General Hospital, Guangdong Academy of Medical Sciences, Guangzhou, Guangdong 510080, P.R. China.
Haike GuoDepartment of Ophthalmology, Guangdong Eye Institute, Guangdong General Hospital, Guangdong Academy of Medical Sciences, Guangzhou, Guangdong 510080, P.R. China.
Lijia XiaoShenzhen Key Laboratory of Ophthalmology, Shenzhen Eye Hospital, Shenzhen, Guangdong 518034, P.R. China.
Xiaohong YangDepartment of Ophthalmology, Guangdong Eye Institute, Guangdong General Hospital, Guangdong Academy of Medical Sciences, Guangzhou, Guangdong 510080, P.R. China.
Ying CuiDepartment of Ophthalmology, Guangdong Eye Institute, Guangdong General Hospital, Guangdong Academy of Medical Sciences, Guangzhou, Guangdong 510080, P.R. China.
Yu HuangDepartment of Ophthalmology, Guangdong Eye Institute, Guangdong General Hospital, Guangdong Academy of Medical Sciences, Guangzhou, Guangdong 510080, P.R. China.
Guangdong General Hospital · CNGuangdong Academy of Medical Sciences · CNSouthern Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The present study aimed to investigate whether the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) signaling pathway is involved in the transforming growth factor β2 (TGF-β2)-induced epithelial-mesenchymal transition (EMT) in human lens epithelial (HLE) cells. HLEB-3 cells were cultured and stimulated with 10 ng/ml TGF-β2 for 24 h. Western blotting was then performed to analyze the expression levels of connexin 43 and fibronectin, and the activities of Akt and mTOR. Confocal cell immunofluorescence was used to observe the expression of phosphorylated (p)-Akt. The toxicity of 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one (LY294002) was assessed using a Cell Counting Kit-8 assay, and inhibition investigations were performed using a PI3K inhibitor. The expression of connexin 43 was suppressed and the expression of fibronectin was increased when the cells were stimulated with 10 ng/ml TGF-β2 for 24 h. In addition, Akt and mTOR were activated during TGF-β2-induced EMT. Treatment of with LY294002 (20 µM) inhibited the activation of Akt and mTOR and effectively prevented TGF-β2-induced EMT in the HLECs. Therefore, the results of the present study indicated that TGF-β2 induces EMT by activating the PI3K/Akt/mTOR signaling pathway in cultured HLECs.

Indexed as

Cell DeathCells, CulturedCell ShapeChromonesEpithelial CellsEpithelial-Mesenchymal TransitionHumansLens, CrystallineMorpholinesPhosphatidylinositol 3-KinasePhosphorylationProto-Oncogene Proteins c-aktSignal TransductionTOR Serine-Threonine KinasesTransforming Growth Factor beta22-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-oneChromonesMorpholinesPhosphatidylinositol 3-KinaseProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesTransforming Growth Factor beta2

Identifiers

PMID26647778
PMCPMC4732853
OpenAlexW2189093799

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.