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Oncogenic fatty acid oxidation senses sleep deficiency-induced circadian disruption to promote tumorigenesis [Ctrl vs SD]

GSE216740 Mus musculus Expression profiling by high throughput sequencing 6 samples Submitted 2025/10/01 Platform GPL24247
Summary
Insufficient sleep and circadian disruption are associated with poor prognosis in cancer patients, yet how sleep deficiency (SD) disrupts circadian cellular biological process that promote tumor growth and development remains elusive. To investigate the effects of sleep deficiency on tumorigenesis, we evaluated the gene expression in the lung from KRASG12D/WT mice after sleep deficient treatment (7 weeks). Analyzing Gene Ontology (GO) Enrichment of significantly up-regulated genes from lung tumors of SD mice, we found that lipid metabolism processes were enriched in the top 20 GO terms. Lipid metabolomics results showed that SD dramatically stimulates fatty acid oxidation process during lung tumorigenesis. Moreover, genetic ablation of ACSL1, a key regulatory factor in FAO, marked reversed SD-promoted lung tumor development. In addition, SD triggered fatty acid oxidation to enhance cancer stem-like properties.
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Direct links to NCBI, no account and no request form: the whole study as GSE216740_RAW.tar, processed values as the series matrix, the supplementary file directory, and per-sample supplementary files for any of the 6 samples. Raw sequencing reads are also available from ENA.

Also filed as BioProject PRJNA895075 and SRA study SRP404938. Searching any of these in the dataset finder brings you back here.

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