Evidence map›Paper›PMID 28588321›Full record

ArticleBritish journal of cancer2017

MicroRNA-199b-5p attenuates TGF-β1-induced epithelial-mesenchymal transition in hepatocellular carcinoma.

Shao-Jun Zhou, Fu-Yao Liu, An-Hong Zhang, Hui-Fang Liang, Ye Wang, Rong Ma, Yuan-Hui Jiang, Nian-Feng Sun

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

36 citing papers in PubMed, 60 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 2 countries.

Shao-Jun ZhouDepartment of General Surgery, Qilu Hospital of Shandong University, 107 West Culture Road, Jinan 250012, China.
Fu-Yao LiuDepartment of Gastrointestinal Medical Oncology, Division of Cancer Medicine, The University of Texas MD Anderson Cancer Center, 7455 Fannin Street, Houston, Texas 77054, USA.
An-Hong ZhangDepartment of General Surgery, Qilu Hospital of Shandong University, 758 Hefei Road, Qingdao 266035, China.
Hui-Fang LiangResearch Laboratory and Hepatic Surgery Center, Department of Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1095 Jie Fang Da Dao, Wuhan 430030, China.
Ye WangDepartment of General Surgery, Qilu Hospital of Shandong University, 758 Hefei Road, Qingdao 266035, China.
Rong MaDepartment of General Surgery, Qilu Hospital of Shandong University, 107 West Culture Road, Jinan 250012, China.
Yuan-Hui JiangDepartment of General Surgery, Qilu Hospital of Shandong University, 758 Hefei Road, Qingdao 266035, China.
Nian-Feng SunDepartment of General Surgery, Qilu Hospital of Shandong University, 107 West Culture Road, Jinan 250012, China.
Qilu Hospital of Shandong University · CNThe University of Texas MD Anderson Cancer Center · USTongji Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAccumulating evidence indicates that N-cadherin is a cell adhesion molecule that has critical roles in tumour progression. However, the role of N-cadherin in hepatocellular carcinoma (HCC) remains controversial.

methodsThis study aims to investigate the expression status of N-cadherin and its molecular mechanisms in HCC.

resultsThe expression of N-cadherin was markedly overexpressed in HCC tissues and cell lines. We identified that miR-199b-5p binds to the 3'-UTR of N-cadherin mRNA, thus decreasing N-cadherin expression in HCC cells. We also found the downregulation of miR-199b-5p in HCC specimens, which was inversely correlated with N-cadherin upregulation, predicted poor clinical outcomes in HCC patients. Next, we determined that miR-199b-5p overexpression promoted cell aggregation, suppressed cell migration and invasion in HCC cells, and inhibited xenografts tumour metastasis in nude mice. Moreover, we demonstrated that miR-199b-5p attenuated TGF-β1 induced epithelial-mesenchymal transition (EMT) -associated traits, while its effects could be partially reversed by N-cadherin restoration. Finally, we examined that N-cadherin downregulation or miR-199b-5p overexpression suppressed TGF-β1-induced Akt phosphorylation, and inhibition of PI3K/Akt pathway blocked TGF-β1-induced N-cadherin overexpression in HCC cells.

conclusionsOur data demonstrate that N-Cadherin was markedly overexpressed and miR-199b-5p was significantly downregulated in HCC. MiR-199b-5p exerts inhibitory effects on EMT, and directly targets N-cadherin in HCC, supporting the potential utility of miR-199b-5p as a promising strategy to treat HCC. Also, a positive regulatory loop exists between N-cadherin and Akt signalling represents a novel mechanism of TGF-β1-mediated EMT in HCC cells.

Indexed as

AnimalsCadherinsCarcinoma, HepatocellularCell MovementEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticHep G2 CellsHumansLiver NeoplasmsMiceMicroRNAsSignal TransductionTransforming Growth Factor beta1Xenograft Model Antitumor AssaysCadherinsMicroRNAsmirn199 microRNA, humanTransforming Growth Factor beta1

Identifiers

PMID28588321
PMCPMC5520514
OpenAlexW2622265135

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.