Evidence map›Paper›PMID 18691339›Full record

ArticleCancer science2008

Bile acids repress E-cadherin through the induction of Snail and increase cancer invasiveness in human hepatobiliary carcinoma.

Koji Fukase, Hideo Ohtsuka, Tohru Onogawa, Hiroshi Oshio, Takayuki Ii, Mitsuhisa Mutoh, Yu Katayose, Toshiki Rikiyama, Masaya Oikawa, Fuyuhiko Motoi and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Cancer science, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing 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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 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
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  12. The role of bile acids in carcinogenesis.Cellular and molecular life sciences : CMLS · 2022
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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

13 authors at 1 institution in 1 country.

Koji FukaseDepartment of Surgery, Tohoku University Graduate School of Medical Science, Sendai 980-8574, Japan.
Hideo Ohtsuka
Tohru Onogawa
Hiroshi Oshio
Takayuki Ii
Mitsuhisa Mutoh
Yu Katayose
Toshiki Rikiyama
Masaya Oikawa
Fuyuhiko Motoi
Shinichi Egawa
Takaaki Abe
Michiaki Unno
Tohoku University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although some kinds of bile acids have been implicated in colorectal cancer development, the mechanism of cancer progression remains unexplored in hepatobiliary cancer. From our personal results using complementary DNA microarray, we found that chenodeoxycholic acid (CDCA) induced Snail expression in human carcinoma cell lines derived from hepatocellular carcinoma and cholangiocarcinoma. Snail expression plays an important role in the regulation of E-cadherin and in the acquisition of invasive potential in many types of human cancers including hepatocellular carcinoma. We found that CDCA and lithocholic acid (LCA) induced Snail expression in a concentration-dependent manner and down-regulated E-cadherin expression in hepatocellular carcinoma and cholangiocarcinoma cell lines. Moreover, Snail short interference RNA (siRNA) treatment reduced the down-regulation of E-cadherin by CDCA or LCA. Luciferase analysis demonstrated that the promoter region from -111 to -24 relative to the transcriptional start site was necessary for this induction and, at least in part, nuclear factor Y (NF-Y) and stimulating protein 1 (Sp1) might be an inducer of Snail expression in response to bile acids. In addition, using an in vitro wound healing assay and invasion assay, we observed that CDCA and LCA induced cell migration and invasion. These results suggest that bile acids repress E-cadherin through the induction of transcription factor Snail and increase cancer invasiveness in human hepatocellular carcinoma and cholangiocarcinoma. Inhibition of this bile acid-stimulated pathway may prove useful as an adjuvant in the therapy of hepatocellular carcinoma.

Indexed as

Bile Duct NeoplasmsBile Ducts, IntrahepaticCadherinsCarcinoma, HepatocellularCell Line, TumorChenodeoxycholic AcidCholangiocarcinomaDown-RegulationFemaleGastrointestinal AgentsHumansLithocholic AcidLiver NeoplasmsMaleNeoplasm InvasivenessSnail Family Transcription FactorsCadherinsChenodeoxycholic AcidGastrointestinal AgentsLithocholic AcidSnail Family Transcription FactorsTranscription Factors

Identifiers

PMID18691339
PMCPMC11160067
OpenAlexW2016639458

What OpenQuestion holds

Textmetadata
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.