Evidence map›Paper›PMID 24484909›Full record

ArticleBMC cancer2014

Metformin anti-tumor effect via disruption of the MID1 translational regulator complex and AR downregulation in prostate cancer cells.

Ummuhan Demir, Andrea Koehler, Rainer Schneider, Susann Schweiger, Helmut Klocker

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

39 citing papers in PubMed, 75 citations in OpenAlex.

  1. Review
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  5. Metformin: A Dual-Role Player in Cancer Treatment and Prevention.International journal of molecular sciences · 2024
    Review
  6. Article
  7. Sexual Dimorphism in Cardiometabolic Diseases: The Role of AMPK.International journal of molecular sciences · 2023
    Review
  8. Review
  9. Review
  10. Article
  11. Article
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  13. Review
  14. Article
  15. Article
  16. Article
  17. Metformin and Malignant Tumors: Not Over the Hill.Diabetes, metabolic syndrome and obesity : targets and therapy · 2021
    Review
  18. Review
  19. Article
  20. 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

5 authors at 3 institutions in 2 countries.

Ummuhan Demir
Andrea Koehler
Rainer Schneider
Susann Schweiger
Helmut KlockerDepartment of Urology, Innsbruck Medical University, 6020 Innsbruck, Austria. helmut.klocker@uki.at.
Innsbruck Medical University · ATUniversität Innsbruck · ATJohannes Gutenberg University Mainz · DE

Funding

Austrian Science Fund FWF TRP 233Austrian Science Fund FWF W 1101
6 · The paper itself

Abstract

backgroundMetformin is an approved drug prescribed for diabetes. Its role as an anti-cancer agent has drawn significant attention because of its minimal side effects and low cost. However, its mechanism of anti-tumour action has not yet been fully clarified.

methodsThe effect on cell growth was assessed by cell counting. Western blot was used for analysis of protein levels, Boyden chamber assays for analyses of cell migration and co-immunoprecipitation (CoIP) followed by western blot, PCR or qPCR for analysis of protein-protein and protein-mRNA interactions.

resultsMetformin showed an anti-proliferative effect on a wide range of prostate cancer cells. It disrupted the AR translational MID1 regulator complex leading to release of the associated AR mRNA and subsequently to downregulation of AR protein in AR positive cell lines. Inhibition of AR positive and negative prostate cancer cells by metformin suggests involvement of additional targets. The inhibitory effect of metformin was mimicked by disruption of the MID1-α4/PP2A protein complex by siRNA knockdown of MID1 or α4 whereas AMPK activation was not required.

conclusionsFindings reported herein uncover a mechanism for the anti-tumor activity of metformin in prostate cancer, which is independent of its anti-diabetic effects. These data provide a rationale for the use of metformin in the treatment of hormone naïve and castration-resistant prostate cancer and suggest AR is an important indirect target of metformin.

Indexed as

Antineoplastic AgentsCell MovementDown-RegulationHumansMaleMetforminMicrotubule ProteinsNuclear ProteinsProstatic NeoplasmsReceptors, AndrogenTranscription FactorsTreatment OutcomeUbiquitin-Protein LigasesAntineoplastic AgentsMetforminMicrotubule ProteinsMID1 protein, humanNuclear ProteinsReceptors, AndrogenTranscription FactorsUbiquitin-Protein Ligases

Identifiers

PMID24484909
PMCPMC3929757
OpenAlexW2030923942

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.