Evidence map›Paper›PMID 25136960›Full record

ArticlePloS one2014

Amygdalin blocks bladder cancer cell growth in vitro by diminishing cyclin A and cdk2.

Jasmina Makarević, Jochen Rutz, Eva Juengel, Silke Kaulfuss, Michael Reiter, Igor Tsaur, Georg Bartsch, Axel Haferkamp, Roman A Blaheta

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
7.9field-weighted citation impact, top 3% 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

32 citing papers in PubMed, 92 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Frontiers in pharmacology · 2024
    Review
  8. Amygdalin Reverses Macrophage PANoptosis Induced by Drug-ResistantJournal of microbiology and biotechnology · 2023
    Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. BioMed research international · 2022
    Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Apoptosis Induction of Armeniacae Semen Extractin Human Acute Leukemia (NALM-6 and KG-1) Cells.International journal of hematology-oncology and stem cell research · 2019
    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

9 authors at 3 institutions in 1 country.

Jasmina MakarevićDepartment of Urology, Goethe University Hospital, Frankfurt am Main, Germany.
Jochen RutzDepartment of Urology, Goethe University Hospital, Frankfurt am Main, Germany.
Eva JuengelDepartment of Urology, Goethe University Hospital, Frankfurt am Main, Germany.
Silke KaulfussInstitute of Human Genetics, University Medical Center Göttingen, Göttingen, Germany.
Michael ReiterDepartment of Urology, Goethe University Hospital, Frankfurt am Main, Germany.
Igor TsaurDepartment of Urology, Goethe University Hospital, Frankfurt am Main, Germany.
Georg BartschDepartment of Urology, Goethe University Hospital, Frankfurt am Main, Germany.
Axel HaferkampDepartment of Urology, Goethe University Hospital, Frankfurt am Main, Germany.
Roman A BlahetaDepartment of Urology, Goethe University Hospital, Frankfurt am Main, Germany.
Goethe University Frankfurt · DEUniversity Hospital Frankfurt · DEUniversitätsmedizin Göttingen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Amygdalin, a natural compound, has been used by many cancer patients as an alternative approach to treat their illness. However, whether or not this substance truly exerts an anti-tumor effect has never been settled. An in vitro study was initiated to investigate the influence of amygdalin (1.25-10 mg/ml) on the growth of a panel of bladder cancer cell lines (UMUC-3, RT112 and TCCSUP). Tumor growth, proliferation, clonal growth and cell cycle progression were investigated. The cell cycle regulating proteins cdk1, cdk2, cdk4, cyclin A, cyclin B, cyclin D1, p19, p27 as well as the mammalian target of rapamycin (mTOR) related signals phosphoAkt, phosphoRaptor and phosphoRictor were examined. Amygdalin dose-dependently reduced growth and proliferation in all three bladder cancer cell lines, reflected in a significant delay in cell cycle progression and G0/G1 arrest. Molecular evaluation revealed diminished phosphoAkt, phosphoRictor and loss of Cdk and cyclin components. Since the most outstanding effects of amygdalin were observed on the cdk2-cyclin A axis, siRNA knock down studies were carried out, revealing a positive correlation between cdk2/cyclin A expression level and tumor growth. Amygdalin, therefore, may block tumor growth by down-modulating cdk2 and cyclin A. In vivo investigation must follow to assess amygdalin's practical value as an anti-tumor drug.

Indexed as

AmygdalinAntineoplastic AgentsCell Cycle CheckpointsCell Line, TumorCell ProliferationCyclin ACyclin-Dependent Kinase 2G1 PhaseHumansProto-Oncogene Proteins c-aktResting Phase, Cell CycleTOR Serine-Threonine KinasesUrinary Bladder NeoplasmsAmygdalinAntineoplastic AgentsCDK2 protein, humanCyclin ACyclin-Dependent Kinase 2MTOR protein, humanProto-Oncogene Proteins c-aktTOR Serine-Threonine Kinases

Identifiers

PMID25136960
PMCPMC4138189
OpenAlexW2027239626

What OpenQuestion holds

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Registered trials

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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.