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2,4-dienoyl-CoA reductase regulates lipid homeostasis in treatment-resistant prostate cancer.

Abstract：

:Despite the clinical success of Androgen Receptor (AR)-targeted therapies, reactivation of AR signalling remains the main driver of castration-resistant prostate cancer (CRPC) progression. In this study, we perform a comprehensive unbiased characterisation of LNCaP cells chronically exposed to multiple AR inhibitors (ARI). Combined proteomics and metabolomics analyses implicate an acquired metabolic phenotype common in ARI-resistant cells and associated with perturbed glucose and lipid metabolism. To exploit this phenotype, we delineate a subset of proteins consistently associated with ARI resistance and highlight mitochondrial 2,4-dienoyl-CoA reductase (DECR1), an auxiliary enzyme of beta-oxidation, as a clinically relevant biomarker for CRPC. Mechanistically, DECR1 participates in redox homeostasis by controlling the balance between saturated and unsaturated phospholipids. DECR1 knockout induces ER stress and sensitises CRPC cells to ferroptosis. In vivo, DECR1 deletion impairs lipid metabolism and reduces CRPC tumour growth, emphasizing the importance of DECR1 in the development of treatment resistance.

journal_name

Nat Commun

journal_title

Nature communications

authors

Blomme A,Ford CA,Mui E,Patel R,Ntala C,Jamieson LE,Planque M,McGregor GH,Peixoto P,Hervouet E,Nixon C,Salji M,Gaughan L,Markert E,Repiscak P,Sumpton D,Blanco GR,Lilla S,Kamphorst JJ,Graham D,Faulds K,MacKay GM,

doi

10.1038/s41467-020-16126-7

subject

Has Abstract

pub_date

2020-05-19 00:00:00

pages

2508

issue

1

issn

2041-1723

pii

10.1038/s41467-020-16126-7

journal_volume

11

pub_type

杂志文章

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