Evidence map›Paper›PMID 29220397›Full record

ArticlePloS one2017

Desethylamiodarone-A metabolite of amiodarone-Induces apoptosis on T24 human bladder cancer cells via multiple pathways.

Zita Bognar, Katalin Fekete, Csenge Antus, Eniko Hocsak, Rita Bognar, Antal Tapodi, Arpad Boronkai, Nelli Farkas, Ferenc Gallyas, Balazs Sumegi and 1 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

14 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Article
  3. Repurposing Amiodarone for Bladder Cancer Treatment.Cancer research communications · 2025
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Biomolecules · 2019
    Article
  11. Article
  12. Review
  13. Article
  14. 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

11 authors at 1 institution in 1 country.

Zita BognarDepartment of Biochemistry and Medical Chemistry, University of Pecs, Pecs, Hungary.ORCID http://orcid.org/0000-0003-0582-7755
Katalin FeketeDepartment of Biochemistry and Medical Chemistry, University of Pecs, Pecs, Hungary.
Csenge AntusDepartment of Biochemistry and Medical Chemistry, University of Pecs, Pecs, Hungary.
Eniko HocsakDepartment of Biochemistry and Medical Chemistry, University of Pecs, Pecs, Hungary.
Rita BognarDepartment of Biochemistry and Medical Chemistry, University of Pecs, Pecs, Hungary.
Antal TapodiDepartment of Biochemistry and Medical Chemistry, University of Pecs, Pecs, Hungary.
Arpad BoronkaiDepartment of Oncotherapy, University of Pecs, Pecs, Hungary.
Nelli FarkasInstitute of Bioanalysis, University of Pecs, Pecs, Hungary.
Ferenc GallyasDepartment of Biochemistry and Medical Chemistry, University of Pecs, Pecs, Hungary.
Balazs SumegiDepartment of Biochemistry and Medical Chemistry, University of Pecs, Pecs, Hungary.
Arpad SzantoDepartment of Urology, University of Pecs, Pecs, Hungary.
University of Pecs · HU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bladder cancer (BC) is a common malignancy of the urinary tract that has a higher frequency in men than in women. Cytostatic resistance and metastasis formation are significant risk factors in BC therapy; therefore, there is great interest in overcoming drug resistance and in initiating research for novel chemotherapeutic approaches. Here, we suggest that desethylamiodarone (DEA)-a metabolite of amiodarone-may have cytostatic potential. DEA activates the collapse of mitochondrial membrane potential (detected by JC-1 fluorescence), and induces cell death in T24 human transitional-cell bladder carcinoma cell line at physiologically achievable concentrations. DEA induces cell cycle arrest in the G0/G1 phase, which may contribute to the inhibition of cell proliferation, and shifts the Bax/Bcl-2 ratio to initiate apoptosis, induce AIF nuclear translocation, and activate PARP-1 cleavage and caspase-3 activation. The major cytoprotective kinases-ERK and Akt-are inhibited by DEA, which may contribute to its cell death-inducing effects. DEA also inhibits the expression of B-cell-specific Moloney murine leukemia virus integration site 1 (BMI1) and reduces colony formation of T24 bladder carcinoma cells, indicating its possible inhibitory effect on metastatic potential. These data show that DEA is a novel anti-cancer candidate of multiple cell death-inducing effects and metastatic potential. Our findings recommend further evaluation of its effects in clinical studies.

Indexed as

AmiodaroneApoptosisCell Line, TumorHumansMembrane Potential, MitochondrialUrinary Bladder NeoplasmsAmiodaronedesethylamiodarone

Identifiers

PMID29220397
PMCPMC5722307
OpenAlexW2774536022

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.