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Transcriptome Analysis of Tumor Associated High Endothelial Venules in Breast Cancer

ABSTRACT: Transcriptome Analysis of Tumor Associated High Endothelial Venules in Breast Cancer

PROVIDER: PRJNA806936 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18016623.fastq.gz	Fastqsanger.gz
	SRR18016624.fastq.gz	Fastqsanger.gz
	SRR18016625.fastq.gz	Fastqsanger.gz
	SRR18016626.fastq.gz	Fastqsanger.gz
	SRR18016627.fastq.gz	Fastqsanger.gz

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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.

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

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

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.

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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.

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Project description:This project aims to characterize the endothelial cell proteome labeled by tumor-derived secreted Sema3C in metastatic lymph nodes using an in vivo TurboID-based proximity labeling strategy. EO771 breast cancer cells overexpressing either a secreted p65-Sema3C–TurboID fusion protein or TurboID alone were orthotopically implanted into C57BL/6 mice. Following tumor growth and lymph node colonization, systemic biotin administration enabled proximity-dependent biotinylation of proteins in neighboring host endothelial cells. Primary high endothelial cells (HECs) were isolated from metastatic lymph nodes, and biotinylated proteins were enriched and analyzed by high-resolution data-independent acquisition (DIA) mass spectrometry. This dataset provides a resource for identifying Sema3C-associated endothelial proteins in the metastatic tumor microenvironment in vivo.

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