Evidence map›Paper›PMID 28197636›Full record

ArticleInternational journal of oncology2017

miR-21 and KLF4 jointly augment epithelial‑mesenchymal transition via the Akt/ERK1/2 pathway.

Chen-Hai Liu, Qiang Huang, Zhi-Yuan Jin, Cheng-Lin Zhu, Zhen Liu, Chao Wang

Open access · hybridAbstract read
In one paragraph

Article in International journal of oncology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

24 citing papers in PubMed, 28 citations in OpenAlex.

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  19. The role of tumour microenvironment: a new vision for cholangiocarcinoma.Journal of cellular and molecular medicine · 2019
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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

6 authors at 2 institutions in 1 country.

Chen-Hai LiuDepartment of General Surgery, Anhui Provincial Hospital of Anhui Medical University, Anhui Key Laboratory of Hepatopancreatobiliary Surgery, Hefei, Anhui 230001, P.R. China.
Qiang HuangDepartment of General Surgery, Anhui Provincial Hospital of Anhui Medical University, Anhui Key Laboratory of Hepatopancreatobiliary Surgery, Hefei, Anhui 230001, P.R. China.
Zhi-Yuan JinDepartment of General Surgery, Anhui Provincial Hospital of Anhui Medical University, Anhui Key Laboratory of Hepatopancreatobiliary Surgery, Hefei, Anhui 230001, P.R. China.
Cheng-Lin ZhuDepartment of General Surgery, Anhui Provincial Hospital of Anhui Medical University, Anhui Key Laboratory of Hepatopancreatobiliary Surgery, Hefei, Anhui 230001, P.R. China.
Zhen LiuDepartment of General Surgery, Anhui Provincial Hospital of Anhui Medical University, Anhui Key Laboratory of Hepatopancreatobiliary Surgery, Hefei, Anhui 230001, P.R. China.
Chao WangDepartment of General Surgery, Anhui Provincial Hospital of Anhui Medical University, Anhui Key Laboratory of Hepatopancreatobiliary Surgery, Hefei, Anhui 230001, P.R. China.
Anhui Medical University · CNAnhui Provincial Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

miR-21 induces epithelial-mesenchymal transition (EMT) of human cholangiocarcinoma (CCA) cells. However, the mechanism by which this occurs remains unclear. In the present study, high throughput platform was employed to detect the genes that are differential expressed in QBC939 cells transfected with a hsa-miR-21 antagomir or control vectors. The EMT-related Krüppel-like factor 4 (KLF4) gene was downregulated after miR-21 was knocked down. Overexpression of miR-21 upregulated KLF4, Akt, ERK and mesenchymal cell markers (N-cadherin and vimentin), downregulated the expression of epithelial cell marker E-cadherin and reduced cell migration and invasion. Immunohistochemistry showed that KLF4, pAkt and pERK were upregulated in tumor xenografts transfected with miR-21 mimics. Inhibitors of the PI3K-Akt and ERK1/2 pathways, LY294002 and U0126, significantly suppressed the EMT phenotype. The present data demonstrated that overexpression of miR-21, accompanied with KLF4, augmented the EMT via inactivation of Akt and ERK1/2 pathways. In conclusion, we have identified a novel mechanism that may be targeted in an attempt to relieve the malignant biological behavior of CCA cells.

Indexed as

Epithelial-Mesenchymal TransitionMAP Kinase Signaling SystemAntigens, CDBile Duct NeoplasmsButadienesCadherinsCell Line, TumorCell MovementCholangiocarcinomaChromonesDown-RegulationEnzyme InhibitorsHumansKruppel-Like Factor 4Kruppel-Like Transcription FactorsMicroRNAs2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-oneAntigens, CDButadienesCadherinsCDH1 protein, humanChromonesEnzyme InhibitorsKLF4 protein, humanKruppel-Like Factor 4Kruppel-Like Transcription FactorsMicroRNAsMIRN21 microRNA, humanMorpholinesNitrilesPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsProto-Oncogene Proteins c-aktU 0126Vimentin

Identifiers

PMID28197636
PMCPMC5363879
OpenAlexW2588901552

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.