Evidence map›Paper›PMID 29568365›Full record

ArticleOncotarget2018

Amiodarone promotes cancer cell death through elevated truncated SRSF3 and downregulation of miR-224.

Yung-Lung Chang, Shu-Ting Liu, Yi-Wen Wang, Wei-Shiang Lin, Shih-Ming Huang

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

19 citing papers in PubMed, 30 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Repurposing Amiodarone for Bladder Cancer Treatment.Cancer research communications · 2025
    Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
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  11. Targeting Ion Channels for Cancer Treatment: Current Progress and Future Challenges.Reviews of physiology, biochemistry and pharmacology · 2022
    Review
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  13. Article
  14. Review
  15. Article
  16. Review
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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

5 authors at 1 institution in 1 country.

Yung-Lung ChangDepartment of Biochemistry, National Defense Medical Center, Taipei City, Taiwan 114, Republic of China.
Shu-Ting LiuDepartment of Biochemistry, National Defense Medical Center, Taipei City, Taiwan 114, Republic of China.
Yi-Wen WangDepartment of Biology and Anatomy, National Defense Medical Center, Taipei City, Taiwan 114, Republic of China.
Wei-Shiang LinDivision of Cardiology, Department of Medicine, Tri-Service General Hospital, National Defense Medical Center, Taipei City, Taiwan 114, Republic of China.
Shih-Ming HuangDepartment of Biochemistry, National Defense Medical Center, Taipei City, Taiwan 114, Republic of China.
National Defense Medical Center · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Amiodarone is a widely used class III antiarrhythmic agent which prolongs the action potential and refractory period by blockage of several types of myocardial potassium channels. Emerging evidence suggests that amiodarone sensitize tumor cells in response to chemotherapy. Nevertheless, little is known about the underlying molecular mechanism. To gain further insight, we demonstrated that amiodarone accumulated the population of a premature termination codon-containing isoform of serine and arginine rich splicing factor 3 (

Indexed as

amiodaroneautophagycaffeinedigoxinmiR-224

Identifiers

PMID29568365
PMCPMC5862586
OpenAlexW2791906251

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.