Evidence map›Paper›PMID 28415688›Full record

ArticleOncotarget2017

Inhibitor SBFI26 suppresses the malignant progression of castration-resistant PC3-M cells by competitively binding to oncogenic FABP5.

Waseem Al-Jameel, Xiaojun Gou, Shiva S Forootan, Majed Saad Al Fayi, Philip S Rudland, Farzad S Forootan, Jiacheng Zhang, Philip A Cornford, Syed A Hussain, Youqiang Ke

Erratum issuedOpen access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
1.3field-weighted citation impact, top 22% 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, 53 citations in OpenAlex.

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  9. A Feedback Loop Between Fatty Acid Metabolism and Epigenetics in Clear Cell Renal Carcinoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 2 institutions in 2 countries.

Waseem Al-JameelMolecular Pathology Laboratory, Department of Molecular and Clinical Cancer Medicine, Liverpool University, Liverpool, L3 9TA, United Kingdom.
Xiaojun GouSichuan Antibiotics Industrial Institute, Chengdu University, Chengdu 610081, China.
Shiva S ForootanMolecular Pathology Laboratory, Department of Molecular and Clinical Cancer Medicine, Liverpool University, Liverpool, L3 9TA, United Kingdom.
Majed Saad Al FayiMolecular Pathology Laboratory, Department of Molecular and Clinical Cancer Medicine, Liverpool University, Liverpool, L3 9TA, United Kingdom.
Philip S RudlandDepartment of Biochemistry, Liverpool University, Liverpool, L69 3GA, United Kingdom.
Farzad S ForootanMolecular Pathology Laboratory, Department of Molecular and Clinical Cancer Medicine, Liverpool University, Liverpool, L3 9TA, United Kingdom.
Jiacheng ZhangMolecular Pathology Laboratory, Department of Molecular and Clinical Cancer Medicine, Liverpool University, Liverpool, L3 9TA, United Kingdom.
Philip A CornfordMolecular Pathology Laboratory, Department of Molecular and Clinical Cancer Medicine, Liverpool University, Liverpool, L3 9TA, United Kingdom.
Syed A HussainMolecular Pathology Laboratory, Department of Molecular and Clinical Cancer Medicine, Liverpool University, Liverpool, L3 9TA, United Kingdom.
Youqiang KeMolecular Pathology Laboratory, Department of Molecular and Clinical Cancer Medicine, Liverpool University, Liverpool, L3 9TA, United Kingdom.
University of Liverpool · GBChengdu University · CN

Funding

Medical Research Council G0801447Medical Research Council MC_PC_14110
6 · The paper itself

Abstract

Castration resistant-prostate cancer is largely impervious to feather hormonal therapy and hence the outlook for patients is grim. Here we use an approach to attach the recently discovered Achilles heel. The experimental treatment established in this study is based on the recent discovery that it is the FABP5-PPARγ-VEGF signalling axis, rather than the androgen receptor pathway, played a dominant role in promoting the malignant progression of castration resistant prostate cancer cells. Treatments have been established in mice by suppressing the biological activity of FABP5 using a chemical inhibitor SBFI26. The inhibitor significantly suppressed the proliferation, migration, invasiveness and colony formation of PC3-M cells in vitro. It also produced a highly significant suppression of both the metastases and the primary tumours developed from cancer cells implanted orthotopically into the prostate glands of the mice. The inhibitor SBFI26 interferes with the FABP5-PPARγ- signalling pathway at the initial stage of the signal transduction by binding competitively to FABP5 to inhibit cellular fatty acid uptake. This avoids the fatty-acid stimulation of PPARγ and prevents it activating the down-stream regulated cancer-promoting genes. This entirely novel experimental approach to treating castration- resistant prostate cancer is completely different from current treatments that are based on androgen-blockade therapy.

Indexed as

AnimalsAntineoplastic AgentsBinding, CompetitiveCell Line, TumorCell MovementCell ProliferationCell SurvivalCyclobutanesDicarboxylic AcidsDisease Models, AnimalDisease ProgressionDrug DiscoveryDrug Screening Assays, AntitumorFatty Acid-Binding ProteinsFatty AcidsHumans1-naphthyl alpha-truxillateAntineoplastic AgentsCyclobutanesDicarboxylic AcidsFABP5 protein, humanFatty Acid-Binding ProteinsFatty AcidsLigandsPPAR gammaCRPCFABP5metastasisPPARγSBFI26

Identifiers

PMID28415688
PMCPMC5458187
OpenAlexW2594632949

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.