Evidence map›Paper›PMID 25955608›Full record

ArticlePloS one2015

Digoxin Suppresses Tumor Malignancy through Inhibiting Multiple Src-Related Signaling Pathways in Non-Small Cell Lung Cancer.

Sheng-Yi Lin, Hsiu-Hui Chang, Yi-Hua Lai, Ching-Hsiung Lin, Min-Hsuan Chen, Gee-Chen Chang, Meng-Feng Tsai, Jeremy J W Chen

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

37 citing papers in PubMed, 70 citations in OpenAlex.

  1. Article
  2. Digoxin and its NaBioorganic & medicinal chemistry · 2024
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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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  15. Article
  16. Review
  17. NaMolecules (Basel, Switzerland) · 2021
    Review
  18. Article
  19. Article
  20. 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

8 authors at 4 institutions in 1 country.

Sheng-Yi LinInstitute of Biomedical Sciences, National Chung Hsing University, Taichung, Taiwan; Agricultural Biotechnology Center, National Chung Hsing University, Taichung, Taiwan.
Hsiu-Hui ChangInstitute of Biomedical Sciences, National Chung Hsing University, Taichung, Taiwan; Division of Chest Medicine, Department of Internal Medicine, Changhua Christian Hospital, Changhua, Taiwan.
Yi-Hua LaiDivision of Chest Medicine, Department of Internal Medicine, Taichung Veterans General Hospital, Taichung, Taiwan.
Ching-Hsiung LinDivision of Chest Medicine, Department of Internal Medicine, Changhua Christian Hospital, Changhua, Taiwan.
Min-Hsuan ChenInstitute of Biomedical Sciences, National Chung Hsing University, Taichung, Taiwan.
Gee-Chen ChangDivision of Chest Medicine, Department of Internal Medicine, Taichung Veterans General Hospital, Taichung, Taiwan.
Meng-Feng TsaiDepartment of Molecular Biotechnology, Dayeh University, Changhua, Taiwan.
Jeremy J W ChenInstitute of Biomedical Sciences, National Chung Hsing University, Taichung, Taiwan; Agricultural Biotechnology Center, National Chung Hsing University, Taichung, Taiwan.
National Chung Hsing University · TWChanghua Christian Hospital · TWTaichung Veterans General Hospital · TWDayeh University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Non-small cell lung cancer is the predominant type of lung cancer, resulting in high mortality worldwide. Digoxin, a cardiac glycoside, has recently been suggested to be a novel chemotherapeutic agent. Src is an oncogene that plays an important role in cancer progression and is therefore a potential target for cancer therapy. Here, we investigated whether digoxin could suppress lung cancer progression through the inhibition of Src activity. The effects of digoxin on lung cancer cell functions were investigated using colony formation, migration and invasion assays. Western blotting and qPCR assays were used to analyze the mRNA and protein expression levels of Src and its downstream proteins, and a cell viability assay was used to measure cellular cytotoxicity effects. The results of the cell function assays revealed that digoxin inhibited the proliferation, invasion, migration, and colony formation of A549 lung cancer cells. Similar effects of digoxin were also observed in other lung cancer cell lines. Furthermore, we found that digoxin significantly suppressed Src activity and its protein expression in a dose- and time-dependent manner as well as reduced EGFR and STAT3 activity. Our data suggest that digoxin is a potential anticancer agent that may suppress lung cancer progression through inhibiting Src and the activity of related proteins.

Indexed as

Signal TransductionAntineoplastic AgentsCarcinoma, Non-Small-Cell LungCell DeathCell Line, TumorCell MovementCell SurvivalDigoxinEnzyme ActivationErbB ReceptorsFocal Adhesion Protein-Tyrosine KinasesGene Expression Regulation, NeoplasticHumansLung NeoplasmsModels, BiologicalNeoplasm InvasivenessAntineoplastic AgentsDigoxinErbB ReceptorsFocal Adhesion Protein-Tyrosine KinasesRNA, Messengersrc-Family KinasesSTAT3 Transcription Factor

Identifiers

PMID25955608
PMCPMC4425490
OpenAlexW1481453425

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.