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Bulk RNA-seq of Kupffer cells from Hepa1-6_EV (empty vector) and Hepa1-6_EpoOE (overexpression) HCC-bearing C57BL/6 mice

GSE290606 Mus musculus Expression profiling by high throughput sequencing 6 samples Submitted 2025/04/30 Platform GPL24247
Summary
Successful cancer immunotherapy requires a patient to mount an effective immune response against tumors, however many cancers evade the body’s immune system. To investigate the basis for treatment failure, we examined spontaneous mouse models of hepatocellular carcinoma (HCC) with either an inflamed T-cell-rich or non-inflamed T-cell-deprived tumor microenvironment (TME). Our studies reveal that erythropoietin (EPO) secreted by tumor cells determines tumor immunotype. Tumor-derived EPO autonomously generates a non-inflamed TME by interacting with its cognate receptor EPOR on tumor-associated macrophages (TAMs). EPO signaling prompts TAMs to become immunoregulatory via NRF2-mediated heme depletion. Removing either tumor-derived EPO or EPOR on TAMs leads to an inflamed TME and tumor regression independent of genotype, due to augmented antitumor T-cell immunity. Thus, the EPO/EPOR axis functions as an immunosuppressive switch for anti-tumor immunity.
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Direct links to NCBI, no account and no request form: the whole study as GSE290606_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 PRJNA1228958 and SRA study SRP566559. Searching any of these in the dataset finder brings you back here.

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