GEO series

Dgat1 detoxifies androgen receptor signaling to promote antitumor CD8+ T cell responses

GSE307220 Mus musculus Expression profiling by high throughput sequencing 4 samples Submitted 2025/12/16 Platform GPL24247

Summary

The role of fatty acid (FA) oxidation 31 in T cell responses has been extensively studied, but whether FA esterification to triacylglycerol (TAG) regulates T cell exhaustion is unknown. Dgat1 catalyzes the rate-limiting step in TAGsynthesis. Here,we showthat deficiency in Dgat1 improvedmitochondrial metabolic fitness and expanded the pool of progenitors of CD8+ exhausted T (Tex) cells to sustain antitumor responses in femalemice. Inmalemice, however, Dgat1 deficiency synergized with androgen receptor (AR) signaling to cause FA peroxidation, endoplasmic reticulum (ER) stress, and Tex cell death. Deletion of Ar, overexpression of glutathione peroxidase 4 (Gpx4), or inhibition of ER stress-induced cell death rescued Dgat1-deficient CD8+ T cell survival and promoted antitumor responses in male mice. This study suggests that Dgat1 detoxifies AR signaling to protect against ER stress-induced cell death and maintain T cell stemness in males, and highlights sex-specific metabolic adaptations in the tumormicroenvironment.

Published in

DGAT1 mediates sex-specific CD8(+) T cell antitumour responses

Madi A, Shi H, Su M et al. · Nature metabolism 2026 · PMID 41862754 · doi:10.1038/s42255-026-01462-7

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Direct links to NCBI, no account and no request form: the whole study as GSE307220_RAW.tar, processed values as the series matrix, the supplementary file directory, and per-sample supplementary files for any of the 4 samples. Raw sequencing reads are also available from ENA.

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Also filed as BioProject PRJNA1314781 and SRA study SRP616978. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 41862754) ↗

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