Evidence map›Paper›PMID 26498355›Full record

ArticleOncotarget2016

FGF19 promotes epithelial-mesenchymal transition in hepatocellular carcinoma cells by modulating the GSK3β/β- catenin signaling cascade via FGFR4 activation.

Huakan Zhao, Fenglin Lv, Guizhao Liang, Xiaobin Huang, Gang Wu, Wenfa Zhang, Le Yu, Lei Shi, Yong Teng

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
4.2field-weighted citation impact, top 5% 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

57 citing papers in PubMed, 102 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

9 authors at 2 institutions in 1 country.

Huakan ZhaoSchool of Life Sciences and School of Bioengineering, Chongqing University, Chongqing, PR China.
Fenglin LvSchool of Life Sciences and School of Bioengineering, Chongqing University, Chongqing, PR China.
Guizhao LiangSchool of Life Sciences and School of Bioengineering, Chongqing University, Chongqing, PR China.
Xiaobin HuangSchool of Life Sciences and School of Bioengineering, Chongqing University, Chongqing, PR China.
Gang WuThird Affiliated Hospital, Third Military Medical University, Chongqing, PR China.
Wenfa ZhangSchool of Life Sciences and School of Bioengineering, Chongqing University, Chongqing, PR China.
Le YuSchool of Life Sciences and School of Bioengineering, Chongqing University, Chongqing, PR China.
Lei ShiSchool of Life Sciences and School of Bioengineering, Chongqing University, Chongqing, PR China.
Yong TengSchool of Life Sciences and School of Bioengineering, Chongqing University, Chongqing, PR China.
Chongqing University · CNDaping Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Compelling evidence suggests that the epithelial-mesenchymal transition (EMT) correlates with aggressiveness of tumors and poor survival. FGF19 has been shown to be involved in EMT in cholangiocarcinoma and colorectal cancer, however, molecular mechanisms underlying FGF19-induced EMT process in hepatocellular carcinoma (HCC) remain largely unknown. Here, we show the expression of FGF19 is significantly elevated and negatively associated with the expression of E-cadherin in HCC tissues and cell lines. Ectopic FGF19 expression promotes EMT and invasion in epithelial-like HCC cells through repression of E-cadherin expression, whereas FGF19 knockdown enhances E-cadherin expression and hence diminishes EMT traits in mesenchymal-like HCC cells, suggesting FGF19 exerts its tumor progressing functions as an EMT inducer. Interestingly, depletion of FGF19 cannot abrogate EMT traits in the presence of GSK3β inhibitors. Furthermore, FGF19-induced EMT can be markedly attenuated when FGFR4 is knocked out. These observations clearly indicate that FGFR4/GSK3β/β-catenin axis may play a pivotal role in FGF19-induced EMT in HCC cells. As FGF19 and its specific receptor FGFR4 are frequently amplified in HCC cells, selective targeting this signaling node may lend insights into a potential effective therapeutic approach for blocking metastasis of HCC.

Indexed as

Epithelial-Mesenchymal TransitionApoptosisbeta CateninBiomarkers, TumorCarcinoma, HepatocellularCase-Control StudiesCell MovementCell ProliferationFibroblast Growth FactorsGlycogen Synthase Kinase 3 betaHumansLiver NeoplasmsPrognosisReceptor, Fibroblast Growth Factor, Type 4Signal TransductionTumor Cells, Culturedbeta CateninBiomarkers, TumorCTNNB1 protein, humanFGF19 protein, humanFGFR4 protein, humanFibroblast Growth FactorsGlycogen Synthase Kinase 3 betaReceptor, Fibroblast Growth Factor, Type 4E-cadherinEMTFGF19FGFR4GSK3β/β-catenin

Identifiers

PMID26498355
PMCPMC4924662
OpenAlexW2209465445

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.