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Androgen receptors promote mitochondrial oxidative phosphorylation, carnitine metabolism, and resistance to palmitate lipotoxicity in ER-mutant breast cancer.

GSE296966 Homo sapiens Expression profiling by high throughput sequencing 6 samples Submitted 2025/12/10 Platform GPL24676
Summary
The effect of androgen receptor (AR) in ER+ breast cancer remains controversial. We find that AR promotes tumor cell growth, oxidative phosphorylation, and fatty acid oxidation under conditions mimicking long-term aromatase inhibition. AR also promotes expression of the mitochondrial and peroxisomal acylcarnitine synthesis enzyme CRAT. AR inhibition decreases CRAT expression and CRAT knockdown is sufficient to inhibit OXPHOS. AR inhibition does not elicit a broad anti-OXPHOS transcriptomic signature, but does affect the expression of a few key metabolic enzymes. AR antagonism also induces a metabolomic signature consistent with severe OXPHOS dysfunction. This work identifies AR as a regulator of CRAT and OXPHOS in ER+ breast cancer.
Published in
Androgen Receptors Promote Oxidative Phosphorylation and Resistance to Palmitate Lipotoxicity in ER-Mutant Breast Cancer
Sessions DT, Boulton DP, Spoelstra NS et al. · Endocrinology 2025 · PMID 41216931 · doi:10.1210/endocr/bqaf168
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Also filed as BioProject PRJNA1262188 and SRA study SRP584828. Searching any of these in the dataset finder brings you back here.

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