Evidence map›Paper›PMID 29958417›Full record

ArticleInternational journal of molecular sciences2018

Farnesoid X Receptor Activation Enhances Transforming Growth Factor β-Induced Epithelial-Mesenchymal Transition in Hepatocellular Carcinoma Cells.

Masahiko Kainuma, Ichiro Takada, Makoto Makishima, Keiji Sano

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
1.1field-weighted citation impact, top 18% 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

32 citing papers in PubMed, 1 synthesis or guideline pooled it, 48 citations in OpenAlex.

  1. Dysregulation of serum bile acids in liver cancer: a systematic review and meta-analysis.Metabolomics : Official journal of the Metabolomic Society · 2025
    Pooled it
  2. Review
  3. Article
  4. Microbiome Modulation withJournal of microbiology and biotechnology · 2026
    Article
  5. Article
  6. Review
  7. Lipids: Driving Forces in the Underlying Biology of Carcinogenesis.ACS pharmacology & translational science · 2025
    Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. The Role of Bile Acids in Pancreatic Cancer.Current cancer drug targets · 2024
    Review
  16. Review
  17. Article
  18. Review
  19. Article
  20. Article
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

4 authors at 2 institutions in 1 country.

Masahiko KainumaDivision of Biochemistry, Department of Biomedical Sciences, Nihon University School of Medicine, 30-1 Oyaguchi-kamicho, Itabashi-ku, Tokyo 173-8610, Japan. kainumamasahiko23@yahoo.co.jp.
Ichiro TakadaDivision of Biochemistry, Department of Biomedical Sciences, Nihon University School of Medicine, 30-1 Oyaguchi-kamicho, Itabashi-ku, Tokyo 173-8610, Japan. takada.ichiro@nihon-u.ac.jp.
Makoto MakishimaDivision of Biochemistry, Department of Biomedical Sciences, Nihon University School of Medicine, 30-1 Oyaguchi-kamicho, Itabashi-ku, Tokyo 173-8610, Japan. makishima.makoto@nihon-u.ac.jp.
Keiji SanoDepartment of Surgery, Teikyo University School of Medicine, 2-11-1 Kaga, Itabashi-ku, Tokyo 173-8605, Japan. k2sano-tky@umin.ac.jp.ORCID 0000-0002-5435-9276
Nihon University · JPTeikyo University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Farnesoid X receptor (FXR) is a receptor for bile acids and plays an important role in the regulation of bile acid metabolism in the liver. Although FXR has been shown to affect hepatocarcinogenesis through both direct and indirect mechanisms, potential roles of FXR in epithelial–mesenchymal transition (EMT) in hepatocellular carcinoma (HCC) remain unclear. We examined the effect of several FXR ligands on EMT-related morphological changes in HCC cell lines, such as HuH-7 and Hep3B cells. FXR agonists (chenodeoxycholic acid, GW4064, and obeticholic acid)—but not an antagonist (guggulsterone)—induced actin polymerization and expression of N-cadherin and phosphorylated focal adhesion kinase, although they were less effective than transforming growth factor β (TGF-β). FXR agonist treatment enhanced TGF-β-induced EMT morphologic changes and FXR antagonist inhibited the effect of TGF-β. Thus, FXR activation enhances EMT in HCC and FXR antagonists may be EMT-suppressing drug candidates.

Indexed as

Bile Acids and SaltsCadherinsCarcinoma, HepatocellularCell Line, TumorChenodeoxycholic AcidEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticHumansIsoxazolesLiverLiver NeoplasmsReceptor, Farnesoid X-ActivatedReceptors, Cytoplasmic and NuclearTransforming Growth Factor beta1Bile Acids and SaltsCadherinsChenodeoxycholic AcidGW 4064Isoxazolesobeticholic acidReceptor, Farnesoid X-ActivatedReceptors, Cytoplasmic and NuclearTransforming Growth Factor beta1bile acidepithelial–mesenchymal transitionfarnesoid X receptorfocal adhesion kinaseguggulsteronehepatocellular carcinomaN-cadherintransforming growth factor β

Identifiers

PMID29958417
PMCPMC6073264
OpenAlexW2811491218

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.