Evidence map›Paper›PMID 19014523›Full record

ArticleBMC cancer2008

Deoxycholic acid induces the overexpression of intestinal mucin, MUC2, via NF-kB signaling pathway in human esophageal adenocarcinoma cells.

Jiantao Wu, Jun Gong, Juan Geng, Yinxue Song

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
1.2field-weighted citation impact, top 21% 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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.

  1. Pooled it
  2. Review
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  10. Review
  11. The role of bile acids in carcinogenesis.Cellular and molecular life sciences : CMLS · 2022
    Review
  12. Article
  13. Article
  14. Article
  15. Using human iPS cell-derived enterocytes as novel in vitro model for the evaluation of human intestinal mucosal damage.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2018
    Article
  16. Article
  17. Review
  18. Article
  19. Bile acid induces MUC2 expression and inhibits tumor invasion in gastric carcinomas.Journal of cancer research and clinical oncology · 2015
    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.

Jiantao WuDepartment of Gastroenterology, the Second Affiliated Hospital, Xi'an Jiaotong University School of Medicine, Xi'an, Shaanxi 710004, PR China. wujjtt@gmail.com
Jun Gong
Juan Geng
Yinxue Song
Second Affiliated Hospital of Xi'an Jiaotong University · CNXi'an Jiaotong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMucin alterations are a common feature of esophageal neoplasia, and alterations in MUC2 mucin have been associated with tumor progression in the esophagus. Bile acids have been linked to esophageal adenocarcinoma and mucin secretion, but their effects on mucin gene expression in human esophageal adenocarcinoma cells is unknown.

methodsHuman esophageal adenocarcinoma cells were treated 18 hours with 50-300 muM deoxycholic acid, chenodeoxycholic acid, or taurocholic acid. MUC2 transcription was assayed using a MUC2 promoter reporter luciferase construct and MUC2 protein was assayed by Western blot analysis. Transcription Nuclear factor-kappaB activity was measured using a Nuclear factor-kappaB reporter construct and confirmed by Western blot analysis for Nuclear factor-kappaB p65.

resultsMUC2 transcription and MUC2 protein expression were increased four to five fold by bile acids in a time and dose-dependent manner with no effect on cell viability. Nuclear factor-kappaB activity was also increased. Treatment with the putative chemopreventive agent aspirin, which decreased Nuclear factor-kappaB activity, also decreased MUC2 transcription. Nuclear factor-kappaB p65 siRNA decreased MUC2 transcription, confirming the significance of Nuclear factor-kappaB in MUC2 induction by deoxycholic acid. Calphostin C, a specific inhibitor of protein kinase C (PKC), greatly decreased bile acid induced MUC2 transcription and Nuclear factor-kappaB activity, whereas inhibitors of MAP kinase had no effect.

conclusionDeoxycholic acid induced MUC2 overexpression in human esophageal adenocarcinoma cells by activation of Nuclear factor-kappaB transcription through a process involving PKC-dependent but not PKA, independent of activation of MAP kinase.

Indexed as

Signal TransductionAdenocarcinomaAnalysis of VarianceAspirinCell Line, TumorChenodeoxycholic AcidCholagogues and CholereticsCyclic AMP-Dependent Protein KinasesDeoxycholic AcidEsophageal NeoplasmsGastrointestinal AgentsGene Expression Regulation, NeoplasticHumansMucin-2NaphthalenesNF-kappa BAspirincalphostin CChenodeoxycholic AcidCholagogues and CholereticsCyclic AMP-Dependent Protein KinasesDeoxycholic AcidGastrointestinal AgentsMUC2 protein, humanMucin-2NaphthalenesNF-kappa BProtein Kinase CRNA, Small InterferingTaurocholic Acid

Identifiers

PMID19014523
PMCPMC2596174
OpenAlexW2146163313

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.