Evidence map›Paper›PMID 25815516›Full record

ArticleInternational journal of oncology2015

Taurolithocholic acid promotes intrahepatic cholangiocarcinoma cell growth via muscarinic acetylcholine receptor and EGFR/ERK1/2 signaling pathway.

Sumet Amonyingcharoen, Tawit Suriyo, Apinya Thiantanawat, Piyajit Watcharasit, Jutamaad Satayavivad

Open access · hybridAbstract read
In one paragraph

Article in International journal of oncology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.3field-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

17 citing papers in PubMed, 35 citations in OpenAlex.

  1. Review
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  5. Article
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  8. Article
  9. The role of bile acids in carcinogenesis.Cellular and molecular life sciences : CMLS · 2022
    Review
  10. Article
  11. Article
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  13. Article
  14. Article
  15. Ilexsaponin AFrontiers in pharmacology · 2021
    Article
  16. Review
  17. 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

5 authors at 2 institutions in 1 country.

Sumet AmonyingcharoenChulabhorn Graduate Institute, Bangkok 10210, Thailand.
Tawit SuriyoLaboratory of Pharmacology, Chulabhorn Research Institute, Bangkok 10210, Thailand.
Apinya ThiantanawatChulabhorn Graduate Institute, Bangkok 10210, Thailand.
Piyajit WatcharasitChulabhorn Graduate Institute, Bangkok 10210, Thailand.
Jutamaad SatayavivadChulabhorn Graduate Institute, Bangkok 10210, Thailand.
Chulabhorn Graduate Institute · THChulabhorn Research Institute · TH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cholangiocarcinoma (CCA) is a malignant cancer of the biliary tract and its occurrence is associated with chronic cholestasis which causes an elevation of bile acids in the liver and bile duct. The present study aimed to investigate the role and mechanistic effect of bile acids on the CCA cell growth. Intrahepatic CCA cell lines, RMCCA-1 and HuCCA-1, were treated with bile acids and their metabolites to determine the growth promoting effect. Cell viability, cell cycle analysis, EdU incorporation assays were conducted. Intracellular signaling proteins were detected by western immunoblotting. Among eleven forms of bile acids and their metabolites, only taurolithocholic acid (TLCA) concentration dependently (1-40 µM) increased the cell viability of RMCCA-1, but not HuCCA-1 cells. The cell cycle analysis showed induction of cells in the S phase and the EdU incorporation assay revealed induction of DNA synthesis in the TLCA-treated RMCCA-1 cells. Moreover, TLCA increased the phosphorylation of EGFR, ERK 1/2 and also increased the expression of cyclin D1 in RMCCA-1 cells. Furthermore, TLCA-induced RMCCA-1 cell growth could be inhibited by atropine, a non-selective muscarinic acetylcholine receptor (mAChR) antagonist, AG 1478, a specific EGFR inhibitor, or U 0126, a specific MEK 1/2 inhibitor. These results suggest that TLCA induces CCA cell growth via mAChR and EGFR/EKR1/2 signaling pathway. Moreover, the functional presence of cholinergic system plays a certain role in TLCA-induced CCA cell growth.

Indexed as

Bile Acids and SaltsBile Duct NeoplasmsCell CycleCell Line, TumorCell SurvivalCholangiocarcinomaCyclin D1ErbB ReceptorsHumansMAP Kinase Signaling SystemPhosphorylationReceptors, MuscarinicTaurolithocholic AcidBile Acids and SaltsCCND1 protein, humanCyclin D1EGFR protein, humanErbB ReceptorsReceptors, MuscarinicTaurolithocholic Acid

Identifiers

PMID25815516
PMCPMC4441291
OpenAlexW2098660828

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.