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

ABSTRACT: 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 further explore potential factor(s) that influence tumor cells, we isolated blood vessel endothelial cells (BECs) in metastatic lymph nodes from six C57BL/6J mice and analyzed them with single-cell RNA sequencing.

ORGANISM(S): Mus musculus

PROVIDER: GSE306742 | GEO | 2026/03/01

REPOSITORIES: GEO

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

Project description: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.

2026-03-01 | GSE245061 | GEO

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

2026-03-01 | GSE217453 | GEO

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

2026-03-01 | GSE216939 | GEO

Transcriptome Analysis of Tumor Associated High Endothelial Venules in Breast Cancer

Project description:High endothelial venules (HEVs) are specialized post-capillary venules that recruit naïve lymphocytes to the lymph nodes and are essential for the development of adaptive immunity. HEVs can also develop in tumors. These specialized tumor vessels are thought to be important for recruiting naïve T cells and B cells into tumors and locally enhancing anti-tumor immunity by supporting the formation of tertiary lymphoid structures. By a comparative transcriptome analysis in human breast cancer, we investigated differentially expressed genes between tumor-associated HEVs and the rest of the tumor vasculature. Tumor vessels highly expressing HEV-upregulated genes, such as the homeobox gene MEOX2 and the tetraspanin gene TSPAN7, were associated with extensive infiltration of T and B lymphocytes and the occurrence of tertiary lymphoid structures, which is known to predict therapeutic responses to immune checkpoint inhibitors. Moreover, high transcript counts of these genes in clinical tumor specimens were associated with a significant survival benefit in advanced breast cancer. The molecular signature of HEVs identified here may be useful for guiding immunotherapies and provide a new direction for investigating tumor-associated HEVs and their clinical significance.

2022-03-31 | GSE196703 | GEO

Single-cell analysis reveals heterogeneity of high endothelial venules and different regulation of genes controlling lymphocyte entry to lymph nodes

Project description:High endothelial venules (HEVs) are specialized blood vessels allowing recirculation of naïve lymphocytes through lymphoid organs. Here, using full length single-cell RNA sequencing, RNA-FISH, flow cytometry and immunohistofluorescence, we reveal the heterogeneity of HEVs in adult mouse peripheral lymph nodes (PLNs) under conditions of homeostasis, antigenic stimulation and after inhibition of lymphotoxin-b receptor (LTbR) signaling. We demonstrate that HEV endothelial cells are in an activated state during homeostasis, and we identify the genes characteristic of the differentiated HEV phenotype. We show that LTbR signaling regulates many HEV genes and pathways in resting PLNs, and that immune stimulation induces a global and temporary inflammatory phenotype in HEVs without compromising their ability to recruit naïve lymphocytes. Most importantly, we uncover differences in the regulation of genes controlling lymphocyte trafficking, Glycam1, Fut7, Gcnt1, Chst4, B3gnt3 and Ccl21a, that have implications for HEV function and regulation in health and disease.

2019-03-12 | GSE106514 | GEO

Effect of recombinant IGLL5 treatment on gene expressing of high endothelial venules

Project description:High endothelial venules (HEVs) are key component in the formation of tertiary lymphatic structure. Our previous studies have shown that IGLL5+B cells adhere to and inhibit the functional phenotype of HEVs. In addition, we found that IGLL5 binds to the LTβR receptor on the membrane of HEVs.

2025-08-01 | GSE272276 | GEO

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

Project description:This SuperSeries is composed of the SubSeries listed below.

2026-03-01 | GSE217454 | GEO

Interferon responsive high endothelial venules drive tumor tertiary lymphoid structure formation and predict response to anti-PD-1 immunotherapy in nasopharyngeal carcinoma

Project description:The outcome of immune checkpoint blockade (ICB) therapy largely hinges on the antitumor immune response of tertiary lymphoid structures (TLSs), but the driver factors behind tumor TLS formation remain poorly understood. Through integrated analysis of spatial and pan-cancer single-cell transcriptomics, we reveal the characteristics of TLSs in nasopharyngeal carcinoma (NPC) and identify a subset of interferon responsive high endothelial venules (IFN-HEVs) that is responsible for the emergence of tumor-specific chemokines, especially CXCL9. Functionally, IFN-HEVs facilitate the recruitment of CD4+ T cells into TLSs via the CXCL9-CXCR3 axis. IFN-HEV-related phenotypes are strongly correlated with positive prognostic outcomes and better responses to ICB therapy. Leveraging these phenotypes, we develop a pretreatment CXCL9-TLS Response-predictive scoring system (CTRscore) to forecast the efficacy of ICB therapy and validate its predictive efficiency in three independent NPC cohorts. Our study provides biological and functional insights into the IFN-HEVs in tumor TLSs, highlighting their potential role in the development of biomarkers and predictors for the success of ICB therapy.

2025-05-02 | GSE289272 | GEO

Comparing the transcriptome expression differences between breast cancer cells EO771-tdT-Parental and EO771-tdT-LM2 using high-throughput sequencing.

Project description:The molecular mechanisms that regulate breast cancer cell (BCC) metastasis and proliferation within the leptomeninges (LM) are poorly understood, limiting development of effective therapies. Here we show that BCCs in mice can invade the LM by abluminal migration along blood vessels that connect vertebral/calvarial bone marrow and meninges, bypassing the blood-brain barrier. To screen for signaling pathways in EO-LM2 cells that could support their survival or proliferation in the meningeal niche, we performed RNA-seq analysis of EO771-tdT-Parental and EO771-tdT-LM2 to compare their transcriptome expression differences.

2025-04-03 | GSE263184 | GEO

Single cell RNA-sequencing of Tumor-Associated High Endothelial Cells (TA-HECs) and comparison to their counterparts in homeostatic and inflamed mouse lymph nodes

Project description:High endothelial venules (HEVs) are specialized postcapillary venules that mediate lymphocyte trafficking from the blood into lymph nodes. HEV-like blood vessels are found in solid tumors in association with CD8+ T cell infiltration.This study uses single cell RNA-sequencing using the Fluidigm C1 system as a method to evaluate the transcriptome in lymph node and tumor-associated HEV endothelial cells (LN-HECs and TA-HECs). We isolated MECA-79+ TA-HECs and CD31+MECA-79- tumor-associated endothelial cells (TA-ECs) by cell sorting and we compared their transcriptome to those of their counterparts in homeostatic (LN-HECs and LN-ECs) or inflamed (iLN-HECs) lymph nodes. TA-HECs express high levels of endothelial cell markers Cdh5 and Pecam1 (CD31), post-capillary venule marker Ackr1 (DARC) and venous transcription factor Nr2f2, indicating that they correspond to post-capillary venule endothelium, like their lymph node counterparts. The genes encoding HEV sialomucins decorated by the sulfated MECA-79 epitope (CD34 and Emcn, endomucin) and the core 1 branching enzyme B3gnt3 that is essential for its biosynthesis, are equally expressed in all HEC populations, whereas sulfotransferases Chst2 and Chst4 are expressed at lower levels in TA-HECs. Although TA-HECs are molecularly distinct from lymph node HECs, they share several important characteristics with iLN-HECs, including the upregulation of endothelial selectins (Selp, Sele) and inflammatory chemokines CXCL9 and CXCL10, the ligands for chemokine receptor CXCR3 on effector T cells. Finally, endothelial cell adhesion molecules ICAM1, ICAM2 and VCAM1 that are important for lymphocyte sticking to HEVs, are expressed at similar levels in all HECs. Together, these findings indicated that MECA-79+ TA-HECs, similar to HECs in immune-stimulated lymph nodes, exhibit an inflamed phenotype characterized by co-expression of MECA-79+ antigens with endothelial selectins and inflammatory chemokines.

2021-12-14 | GSE154898 | GEO

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