Evidence map›Paper›PMID 28970500›Full record

ArticleScientific reports2017

The FXR Agonist, Obeticholic Acid, Suppresses HCC Proliferation & Metastasis: Role of IL-6/STAT3 Signalling Pathway.

Yasmeen M Attia, Rasha A Tawfiq, Aya A Ali, Mohamed M Elmazar

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed, 1 pooled it
1.8field-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

51 citing papers in PubMed, 1 synthesis or guideline pooled it, 74 citations in OpenAlex.

  1. Pharmacological Mechanisms of Bile Acids Targeting the Farnesoid X Receptor.International journal of molecular sciences · 2024
    Pooled it
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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

4 authors at 1 institution in 1 country.

Yasmeen M AttiaDepartment of Pharmacology, The Center for Drug Research and Development (CDRD), Faculty of Pharmacy, The British University in Egypt, El Sherouk City, P.O. Box 43, Cairo, 11837, Egypt. yasmeen.attia@bue.edu.eg.
Rasha A TawfiqDepartment of Pharmacology, The Center for Drug Research and Development (CDRD), Faculty of Pharmacy, The British University in Egypt, El Sherouk City, P.O. Box 43, Cairo, 11837, Egypt.
Aya A AliDepartment of Pharmacology, The Center for Drug Research and Development (CDRD), Faculty of Pharmacy, The British University in Egypt, El Sherouk City, P.O. Box 43, Cairo, 11837, Egypt.
Mohamed M ElmazarDepartment of Pharmacology, The Center for Drug Research and Development (CDRD), Faculty of Pharmacy, The British University in Egypt, El Sherouk City, P.O. Box 43, Cairo, 11837, Egypt.
British University in Egypt · EG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The nuclear receptor, farnesoid X receptor (FXR), has been recently considered as a tumor suppressor in HCC. IL-6/Janus kinase 2 (Jak-2)/signal transducer and activator of transcription 3 (STAT3) pathway has been implicated as a key player in many cancer types. This study aimed at investigating the potential effect of the FXR agonist, obeticholic acid (OCA), on HCC and the involvement of IL-6/STAT3 pathway. The potential regulation of STAT3 by its main feedback inhibitor target gene, the suppressor of cytokine signaling 3 (SOCS3), triggered by OCA was also explored. Cytotoxicity studies were performed on HepG2, Huh7, and SNU-449 cell lines using OCA alone and combined with the FXR antagonist guggulsterone (Gugg). OCA cytotoxic effect was significantly hampered in presence of Gugg. OCA also caused cell cycle arrest and inhibited invasion and migration of HCC cells. Decrease in STAT3 phosphorylation and SOCS3 upregulation were also observed. Moreover, Jak-2, IL-1β, and IL-6 levels were decreased. These results were correlated with an upregulation of FXR and small heterodimer partner (SHP) levels. Effects of OCA on IL-6/STAT3 main key players were reversed in presence of Gugg. Overall, these findings suggest a potential effect of OCA in HCC via interfering with IL-6/STAT3 signalling pathway in vitro.

Indexed as

Gene Expression Regulation, NeoplasticAntineoplastic Agents, PhytogenicCell Cycle CheckpointsCell Line, TumorCell MovementCell ProliferationChenodeoxycholic AcidHepatocytesHep G2 CellsHumansInterleukin-1betaInterleukin-6Janus Kinase 2PregnenedionesReceptor, Farnesoid X-ActivatedReceptors, Cytoplasmic and NuclearAntineoplastic Agents, PhytogenicChenodeoxycholic AcidIL1B protein, humanIL6 protein, humanInterleukin-1betaInterleukin-6JAK2 protein, humanJanus Kinase 2nuclear receptor subfamily 0, group B, member 2obeticholic acidpregna-4,17-diene-3,16-dionePregnenedionesReceptor, Farnesoid X-ActivatedReceptors, Cytoplasmic and NuclearSOCS3 protein, humanSTAT3 protein, humanSTAT3 Transcription FactorSuppressor of Cytokine Signaling 3 Protein

Identifiers

PMID28970500
PMCPMC5624958
OpenAlexW2760388735

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.