Evidence map›Paper›PMID 40175359›Full record

ArticleCell death discovery2025

Ursodeoxycholic acid prompts glycolytic dominance, reductive stress and epithelial-to-mesenchymal transition in ovarian cancer cells through NRF2 activation.

Adrienn Sipos, Éva Kerekes, Dóra Szeőcs, Fanni Szarvas, Szandra Schwarcz, Emese Tóth, Gyula Ujlaki, Edit Mikó, Peter Bai

Abstract read
In one paragraph

Article in Cell death discovery, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. Review
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

9 authors.

Adrienn SiposDepartment of Medical Chemistry, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Éva KerekesDepartment of Medical Chemistry, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Dóra SzeőcsDepartment of Medical Chemistry, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Fanni SzarvasDepartment of Medical Chemistry, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Szandra SchwarczDepartment of Medical Chemistry, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Emese TóthDepartment of Medical Chemistry, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Gyula UjlakiDepartment of Medical Chemistry, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Edit MikóDepartment of Medical Chemistry, Faculty of Medicine, University of Debrecen, Debrecen, Hungary. miko.edit@med.unideb.hu.ORCID http://orcid.org/0000-0001-7584-445X
Peter BaiDepartment of Medical Chemistry, Faculty of Medicine, University of Debrecen, Debrecen, Hungary. baip@med.unideb.hu.ORCID http://orcid.org/0000-0002-6191-6616

Funding

Nemzeti Kutatási, Fejlesztési és Innovációs Hivatal (NKFI Office) FK 128 387Nemzeti Kutatási, Fejlesztési és Innovációs Hivatal (NKFI Office) FK146 852Nemzeti Kutatási, Fejlesztési és Innovációs Hivatal (NKFI Office) K142141
6 · The paper itself

Abstract

Numerous secreted bacterial metabolites were identified with bioactivity in various neoplasias, including ovarian cancer. One such metabolite is ursodeoxycholic acid (UDCA), a secondary bile acid that has widespread beneficial effects in neoplasias. Hereby, we assessed the bioactivity of UDCA in cell models of ovarian cancer, by applying UDCA in concentrations corresponding to the serum reference concentrations of UDCA (300 nM). UDCA induced epithelial-to-mesenchymal transition (EMT), increased the flux of glycolysis and reduced the naturally occurring oxidative stress in ovarian cancer cells. These changes were dependent on the activation of NRF2. The tumoral overexpression of UDCA-induced genes in humans correlated with worse survival. These results point out that bacterial metabolites may have opposite effects in different neoplasias and raise the possibility that UDCA-containing remedies on the long run may support cancer progression in ovarian cancer patients.

Identifiers

PMID40175359
PMCPMC11965337

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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.