Evidence map›Paper›PMID 30905848›Full record

ArticleEBioMedicine2019

Discovery of therapeutic agents for prostate cancer using genome-scale metabolic modeling and drug repositioning.

Beste Turanli, Cheng Zhang, Woonghee Kim, Rui Benfeitas, Mathias Uhlen, Kazim Yalcin Arga, Adil Mardinoglu

Open access · goldAbstract read
In one paragraph

Article in EBioMedicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
11.6field-weighted citation impact, top 1% 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

41 citing papers in PubMed, 93 citations in OpenAlex.

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  8. Genome-scale models in human metabologenomics.Nature reviews. Genetics · 2025
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  10. Frontiers in pharmacology · 2024
    Article
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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

7 authors at 3 institutions in 3 countries.

Beste TuranliScience for Life Laboratory, KTH - Royal Institute of Technology, Stockholm SE-17121, Sweden; Department of Bioengineering, Marmara University, Istanbul, Turkey; Department of Bioengineering, Istanbul Medeniyet University, Istanbul, Turkey.
Cheng ZhangScience for Life Laboratory, KTH - Royal Institute of Technology, Stockholm SE-17121, Sweden.
Woonghee KimScience for Life Laboratory, KTH - Royal Institute of Technology, Stockholm SE-17121, Sweden.
Rui BenfeitasScience for Life Laboratory, KTH - Royal Institute of Technology, Stockholm SE-17121, Sweden.
Mathias UhlenScience for Life Laboratory, KTH - Royal Institute of Technology, Stockholm SE-17121, Sweden.
Kazim Yalcin ArgaDepartment of Bioengineering, Marmara University, Istanbul, Turkey. Electronic address: kazim.arga@marmara.edu.tr.
Adil MardinogluScience for Life Laboratory, KTH - Royal Institute of Technology, Stockholm SE-17121, Sweden; Department of Biology and Biological Engineering, Chalmers University of Technology, Gothenburg SE-41296, Sweden; Centre for Host-Microbiome Interactions, Faculty of Dentistry, Oral & Craniofacial Sciences, King's College London, London, United Kingdom. Electronic address: adilm@scilifelab.se.
Science for Life Laboratory · SEKing's College London · GBMarmara University · TR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundGenome-scale metabolic models (GEMs) offer insights into cancer metabolism and have been used to identify potential biomarkers and drug targets. Drug repositioning is a time- and cost-effective method of drug discovery that can be applied together with GEMs for effective cancer treatment.

methodsIn this study, we reconstruct a prostate cancer (PRAD)-specific GEM for exploring prostate cancer metabolism and also repurposing new therapeutic agents that can be used in development of effective cancer treatment. We integrate global gene expression profiling of cell lines with >1000 different drugs through the use of prostate cancer GEM and predict possible drug-gene interactions.

findingsWe identify the key reactions with altered fluxes based on the gene expression changes and predict the potential drug effect in prostate cancer treatment. We find that sulfamethoxypyridazine, azlocillin, hydroflumethiazide, and ifenprodil can be repurposed for the treatment of prostate cancer based on an in silico cell viability assay. Finally, we validate the effect of ifenprodil using an in vitro cell assay and show its inhibitory effect on a prostate cancer cell line.

interpretationOur approach demonstate how GEMs can be used to predict therapeutic agents for cancer treatment based on drug repositioning. Besides, it paved a way and shed a light on the applicability of computational models to real-world biomedical or pharmaceutical problems.

Indexed as

Drug DiscoveryDrug RepositioningGenome, HumanGenomicsMetabolomicsCell Line, TumorCell SurvivalGene Expression ProfilingGenes, ReporterHumansMaleMetabolic Networks and PathwaysPiperidinesProstatic NeoplasmsProteomeProteomicsifenprodilPiperidinesProteomeApproved drugsDrug repositioningDrug repurposingGenome-scale metabolic modelsProstate cancer

Identifiers

PMID30905848
PMCPMC6491384
OpenAlexW2923278922

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.