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Tumour-associated high endothelial venules drive portal-specific immune evasion in lymph nodes via ALOX12 [III]

GSE245061 Mus musculus Expression profiling by high throughput sequencing 8 samples Submitted 2026/03/01 Platform GPL24247
Summary
High-endothelial-venules (HEVs) offer another entry point for tumor metastasis in mice. To investigate whether HEVs and non-specialized blood vessels exert different effects on disseminating tumor cells, we enriched EO771 derivatives HEVM3 (preferentially metastasize through HEVs) cells and BVM3 (preferentially metastasize through blood vessels) cells. To explore how HEVs regulate immunogenicity of tumor cells, we compared the transcriptomes of BECs isolated from mammary blood vessels and HECs isolated from lymph nodes of mice inoculated with or without EO771-HEVM3 tumors. We demonstrated that ALOX12 specifically expressed in HEVs in LNs induces immune evasion of neighboring tumor cells by 12-HETE. To identify the factor(s) that upregulate ALOX12, we compared the mRNA transcriptomes between EO771-HEVM3 cells and EO771-BVM3 cells. To explore how 12-HETE promotes immune evasion of tumor cells, we performed total RNA-seq analysis in EO771 cells after 12-HETE treatment.
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Direct links to NCBI, no account and no request form: the whole study as GSE245061_RAW.tar, processed values as the series matrix, the supplementary file directory, and per-sample supplementary files for any of the 8 samples. Raw sequencing reads are also available from ENA.

Also filed as BioProject PRJNA1026880 and SRA study SRP465622. Searching any of these in the dataset finder brings you back here.

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