Evidence map›Paper›PMID 38216720›Full record

ArticleBritish journal of cancer2024

Peroxisomal β-oxidation enzyme, DECR2, regulates lipid metabolism and promotes treatment resistance in advanced prostate cancer.

Chui Yan Mah, An Dieu Trang Nguyen, Takuto Niijima, Madison Helm, Jonas Dehairs, Feargal J Ryan, Natalie Ryan, Lake-Ee Quek, Andrew J Hoy, Anthony S Don and 5 more

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

17 citing papers in PubMed, 18 citations in OpenAlex.

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  10. Metabolic phenotypes and fatty acid profiles associated with histopathology of primary aldosteronism.Hypertension research : official journal of the Japanese Society of Hypertension · 2025
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  14. Frontiers in pharmacology · 2025
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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

15 authors at 6 institutions in 3 countries.

Chui Yan MahSouth Australian Immunogenomics Cancer Institute and Freemasons Centre for Male Health and Wellbeing, University of Adelaide, Adelaide, SA, Australia.
An Dieu Trang NguyenSouth Australian Immunogenomics Cancer Institute and Freemasons Centre for Male Health and Wellbeing, University of Adelaide, Adelaide, SA, Australia.
Takuto NiijimaSouth Australian Immunogenomics Cancer Institute and Freemasons Centre for Male Health and Wellbeing, University of Adelaide, Adelaide, SA, Australia.
Madison HelmSouth Australian Immunogenomics Cancer Institute and Freemasons Centre for Male Health and Wellbeing, University of Adelaide, Adelaide, SA, Australia.
Jonas DehairsDepartment of Oncology, Laboratory of Lipid Metabolism and Cancer, KU Leuven, Leuven, Belgium.ORCID 0000-0002-6789-2264
Feargal J RyanPrecision Cancer Medicine Theme, South Australian Health and Medical Research Institute, Adelaide, SA, Australia.ORCID 0000-0002-1565-4598
Natalie RyanSouth Australian Immunogenomics Cancer Institute and Freemasons Centre for Male Health and Wellbeing, University of Adelaide, Adelaide, SA, Australia.
Lake-Ee QuekSchool of Medical Sciences, Charles Perkins Centre, Faculty of Medicine and Health, University of Sydney, Camperdown, NSW, 2006, Australia.
Andrew J HoySchool of Medical Sciences, Charles Perkins Centre, Faculty of Medicine and Health, University of Sydney, Camperdown, NSW, 2006, Australia.ORCID 0000-0003-3922-1137
Anthony S DonSchool of Medical Sciences, Charles Perkins Centre, Faculty of Medicine and Health, University of Sydney, Camperdown, NSW, 2006, Australia.
Ian G MillsPatrick G Johnston Centre for Cancer Research, Queen's University, Belfast, UK.
Johannes V SwinnenDepartment of Oncology, Laboratory of Lipid Metabolism and Cancer, KU Leuven, Leuven, Belgium.ORCID 0000-0002-7720-5077
David J LynnPrecision Cancer Medicine Theme, South Australian Health and Medical Research Institute, Adelaide, SA, Australia.ORCID 0000-0003-4664-1404
Zeyad D NassarSouth Australian Immunogenomics Cancer Institute and Freemasons Centre for Male Health and Wellbeing, University of Adelaide, Adelaide, SA, Australia. zeyad.nassar@adelaide.edu.au.
Lisa M ButlerSouth Australian Immunogenomics Cancer Institute and Freemasons Centre for Male Health and Wellbeing, University of Adelaide, Adelaide, SA, Australia. lisa.butler@adelaide.edu.au.ORCID 0000-0003-2698-3220
South Australian Health and Medical Research Institute · AUThe University of Sydney · AUFlinders University · AUVIB-KU Leuven Center for Cancer Biology · BEQueen's University Belfast · GBThe University of Adelaide · AU

Funding

Cancer Australia ID2011672Cancer Council South Australia PRF1117Hospital Research Foundation (The Hospital Research Foundation) C-PJ-10-Prost-2020KU Leuven (Katholieke Universiteit Leuven) C14/21/095Movember Foundation (Movember) MRTA3Prostate Cancer Foundation of Australia (PCFA) Future Leaders AwardStichting Tegen Kanker (Belgian Foundation Against Cancer) F/2020/1417University of Adelaide International PhD Scholarship
6 · The paper itself

Abstract

backgroundPeroxisomes are central metabolic organelles that have key roles in fatty acid homoeostasis. As prostate cancer (PCa) is particularly reliant on fatty acid metabolism, we explored the contribution of peroxisomal β-oxidation (perFAO) to PCa viability and therapy response.

methodsBioinformatic analysis was performed on clinical transcriptomic datasets to identify the perFAO enzyme, 2,4-dienoyl CoA reductase 2 (DECR2) as a target gene of interest. Impact of DECR2 and perFAO inhibition via thioridazine was examined in vitro, in vivo, and in clinical prostate tumours cultured ex vivo. Transcriptomic and lipidomic profiling was used to determine the functional consequences of DECR2 inhibition in PCa.

resultsDECR2 is upregulated in clinical PCa, most notably in metastatic castrate-resistant PCa (CRPC). Depletion of DECR2 significantly suppressed proliferation, migration, and 3D growth of a range of CRPC and therapy-resistant PCa cell lines, and inhibited LNCaP tumour growth and proliferation in vivo. DECR2 influences cell cycle progression and lipid metabolism to support tumour cell proliferation. Further, co-targeting of perFAO and standard-of-care androgen receptor inhibition enhanced suppression of PCa cell proliferation.

conclusionOur findings support a focus on perFAO, specifically DECR2, as a promising therapeutic target for CRPC and as a novel strategy to overcome lethal treatment resistance.

Indexed as

Prostatic Neoplasms, Castration-ResistantAndrogensCell Line, TumorCell ProliferationFatty AcidsHumansLipid MetabolismMaleReceptors, AndrogenAndrogensFatty AcidsReceptors, Androgen

Identifiers

PMID38216720
PMCPMC10912652
OpenAlexW4390829154

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.