Evidence map›Paper›PMID 40790066›Full record

ArticleScientific reports2025

Dysregulation of bile acid metabolism in patients with colorectal cancer.

Su-Mi Lee, Seon-Young Park, Khom Sophallika, Jin Ook Chung, Yong Wook Jung, Dong Hyun Kim, Jin Won Kim, Hyun Soo Kim, Jae Hyun Yoon, Young Do Jung and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Bile acid signaling in health and disease.Molecular biomedicine · 2026
    Review
  2. Review
  3. 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

13 authors.

Su-Mi LeeDepartment of Internal Medicine, Chonnam National University Medical School, Gwangju, South Korea.
Seon-Young ParkDepartment of Internal Medicine, Chonnam National University Medical School, Gwangju, South Korea. drpsy@naver.com.
Khom SophallikaDepartment of Internal Medicine, Chonnam National University Medical School, Gwangju, South Korea.
Jin Ook ChungDepartment of Internal Medicine, Chonnam National University Medical School, Gwangju, South Korea.
Yong Wook JungDepartment of Internal Medicine, Chonnam National University Medical School, Gwangju, South Korea.
Dong Hyun KimDepartment of Internal Medicine, Chonnam National University Medical School, Gwangju, South Korea.
Jin Won KimDepartment of Internal Medicine, Chonnam National University Medical School, Gwangju, South Korea.
Hyun Soo KimDepartment of Internal Medicine, Chonnam National University Medical School, Gwangju, South Korea.
Jae Hyun YoonDepartment of Internal Medicine, Chonnam National University Medical School, Gwangju, South Korea.
Young Do JungDepartment of Biochemistry, Chonnam National University Medical School, Gwangju, South Korea.
Jae Kyun JuDepartment of General Surgery, Chonnam National University Medical School, Gwangju, South Korea.
Jun Seong ChungDepartment of General Surgery, Chonnam National University Medical School, Gwangju, South Korea.
Han Deok KwakDepartment of General Surgery, Chonnam National University Medical School, Gwangju, South Korea.

Funding

Chonnam National University Hospital Biomedical Research Institute BCRI23016National Research Foundation of Korea NRF-2021R1F1A1059503National Research Foundation of Korea RS-2023-00244540
6 · The paper itself

Abstract

Bile acid (BA) metabolism and signaling may influence cancer risk. We investigated differences in circulating BA composition between healthy controls and patients with colorectal cancer (CRC) and assessed the epithelial-mesenchymal transition (EMT) in CRC cell lines exposed to chenodeoxycholic acid (CDCA). BA, C4, and fibroblast growth factor-19 (FGF19) concentrations in serum samples from 70 controls and 133 patients with CRC were analyzed. Results showed that primary and secondary BAs, C4, and FGF19 were significantly lower in CRC patients than in the age- and sex- matched controls (P < 0.05). CDCA reduced the percentage of EdU-positive cells in HCT116 and HT-29 cells by 53.6% and 28.3%, respectively (P < 0.001) and decreased the rate of wound closure by 0.31 ± 0.05- and 0.30 ± 0.06-fold in HCT116 and HT-29 cells, respectively(P < 0.05). It significantly reduced spheroid formation by 90.0% and 94.3% in HCT116 and HT-29 cells, respectively (P < 0.0001) and downregulated EMT-related stem cell markers in CRC cells. The dysregulation of BA synthesis and recycling might contribute to CRC carcinogenesis. CDCA might alter EMT, protecting against CRC development and progression. The predictive role of plasma BAs in CRC prognosis and their potential in CRC prevention and management should be further explored.

Indexed as

Bile Acids and SaltsColorectal NeoplasmsAgedCase-Control StudiesChenodeoxycholic AcidEpithelial-Mesenchymal TransitionFemaleFibroblast Growth FactorsHCT116 CellsHT29 CellsHumansMaleMiddle AgedBile Acids and SaltsChenodeoxycholic AcidFGF19 protein, humanFibroblast Growth FactorsBile acidsChenodeoxycholic acidColorectal cancerEpithelial–mesenchymal transition

Identifiers

PMID40790066
PMCPMC12340127

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.