Evidence map›Paper›PMID 37145211›Full record

ArticleMolecular biology reports2023

The pro- and antineoplastic effects of deoxycholic acid in pancreatic adenocarcinoma cell models.

Szandra Schwarcz, Patrik Kovács, Tünde Kovács, Gyula Ujlaki, Petra Nyerges, Karen Uray, Péter Bai, Edit Mikó

Open access · hybridAbstract read
In one paragraph

Article in Molecular biology reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

8 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. The Role of Bile Acids in Pancreatic Cancer.Current cancer drug targets · 2024
    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

8 authors at 1 institution in 1 country.

Szandra Schwarcz *Department of Medical Chemistry, University of Debrecen, Egyetem Tér 1., Debrecen, 4032, Hungary.
Patrik Kovács *Department of Medical Chemistry, University of Debrecen, Egyetem Tér 1., Debrecen, 4032, Hungary.
Tünde KovácsDepartment of Medical Chemistry, University of Debrecen, Egyetem Tér 1., Debrecen, 4032, Hungary.
Gyula UjlakiDepartment of Medical Chemistry, University of Debrecen, Egyetem Tér 1., Debrecen, 4032, Hungary.
Petra NyergesDepartment of Medical Chemistry, University of Debrecen, Egyetem Tér 1., Debrecen, 4032, Hungary.
Karen UrayDepartment of Medical Chemistry, University of Debrecen, Egyetem Tér 1., Debrecen, 4032, Hungary.
Péter BaiDepartment of Medical Chemistry, University of Debrecen, Egyetem Tér 1., Debrecen, 4032, Hungary. baip@med.unideb.hu.
Edit MikóDepartment of Medical Chemistry, University of Debrecen, Egyetem Tér 1., Debrecen, 4032, Hungary. miko.edit@med.unideb.hu.ORCID http://orcid.org/0000-0001-7584-445X
University of Debrecen · HU

Funding

Hungarian Academy of Sciences POST-COVID2021-33New National Excellence Program of the Ministry of Human Capacities ÚNKP-20-3-I-DE-301New National Excellence Program of the Ministry of Human Capacities ÚNKP-21-3-I-DE-105New National Excellence Program of the Ministry of Human Capacities ÚNKP-22-3-II-DE-230NKFIH FK128387NKFIH K124141NKFIH TKP2021-EGA-19NKFIH TKP2021-EGA-20
6 · The paper itself

Abstract

backgroundCommensal bacteria secrete metabolites that reach distant cancer cells through the circulation and influence cancer behavior. Deoxycholic acid (DCA), a hormone-like metabolite, is a secondary bile acid specifically synthesized by intestinal microbes. DCA may have both pro- and antineoplastic effects in cancers. METHODS AND

resultsThe pancreatic adenocarcinoma cell lines, Capan-2 and BxPC-3, were treated with 0.7 µM DCA, which corresponds to the reference concentration of DCA in human serum. DCA influenced the expression of epithelial to mesenchymal transition (EMT)-related genes, significantly decreased the expression level of the mesenchymal markers, transcription factor 7- like 2 (TCF7L2), snail family transcriptional repressor 2 (SLUG), CLAUDIN-1, and increased the expression of the epithelial genes, zona occludens 1 (ZO-1) and E-CADHERIN, as shown by real-time PCR and Western blotting. Consequently, DCA reduced the invasion capacity of pancreatic adenocarcinoma cells in Boyden chamber experiments. DCA induced the protein expression of oxidative/nitrosative stress markers. Moreover, DCA reduced aldehyde dehydrogenase 1 (ALDH1) activity in an Aldefluor assay and ALDH1 protein level, suggesting that DCA reduced stemness in pancreatic adenocarcinoma. In Seahorse experiments, DCA induced all fractions of mitochondrial respiration and glycolytic flux. The ratio of mitochondrial oxidation and glycolysis did not change after DCA treatment, suggesting that cells became hypermetabolic.

conclusionDCA induced antineoplastic effects in pancreatic adenocarcinoma cells by inhibiting EMT, reducing cancer stemness, and inducing oxidative/nitrosative stress and procarcinogenic effects such as hypermetabolic bioenergetics.

Indexed as

AdenocarcinomaAntineoplastic AgentsPancreatic NeoplasmsCell Line, TumorDeoxycholic AcidEpithelial-Mesenchymal TransitionHumansAntineoplastic AgentsDeoxycholic AcidCell metabolismDCAEMTOxidative/nitrosative stressPancreatic adenocarcinomaStemness

Identifiers

PMID37145211
PMCPMC10209225
OpenAlexW4372286564

What OpenQuestion holds

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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.