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Transcriptomic profiling of metastasis-associated lung endothelial cells from mice treated with anti-VEGFR2 antibody (DC101)

ABSTRACT: Transcriptomic profiling of metastasis-associated lung endothelial cells from mice treated with anti-VEGFR2 antibody (DC101)

PROVIDER: PRJNA657597 | ENA |

REPOSITORIES: ENA

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Transcriptomic profiling of metastasis-associated lung endothelial cells from mice treated with anti-VEGFR2 antibody (DC101)

Project description:In cancer progression to metastasis, disseminated cancer cells frequently lodge near vasculature in secondary organs. However, our understanding of the cellular crosstalk evoked at perivascular sites is still rudimentary. In this study, we identified an inter-cellular machinery governing formation of a pro-metastatic vascular niche during breast cancer colonization in lungs. Transcriptomic analysis of endothelial cells (ECs) isolated from mouse lungs with metastases revealed a marked upregulation of genes linked to proliferation, inflammation and numerous secreted proteins. We showed that four secreted factors, INHBB, SCGB3A1, OPG and LAMA1, induced in ECs form a supportive niche that promotes metastasis in mice, by enhancing stem cell properties and survival ability of cancer cells. Interestingly, the blocking vascular endothelial cell growth factor (VEGF), a major cytokine regulating EC behaviors, dramatically suppressed EC proliferation whereas no impact was observed on the expression of the four vascular niche factors in lung ECs. We found that the formation of a vascular niche is correlated with inflammation, and revealed that metastasis-associated macrophages are essential for production of all of four niche factors in lung ECs. Macrophages are activated via TNC-TLR4 at perivasculature and sequentially stimulate ECs to produce the four niche factors. Thus, our findings provide mechanistic insights into the formation of a perivascular niche and offer the possibility that targeting macrophages may synergize with existing anti-angiogenic drugs to effectively suppress vascular function in metastatic colonization. We used microarrays to analyze the global changes of gene expression in metastasis-associated lung endothelial cells upon VEGFR2 inhibition

2021-12-31 | GSE156350 | GEO

Gene expression data of MKN45 xenograft tumors treated with anti-VEGFR2 and anti-VEGF-A antibodies

Project description:The vascular endothelial growth factor (VEGF) /VEGF receptor (VEGFR) axis is an essential regulator of angiogenesis and important therapeutic target in cancer. However, the efficacy of combination treatment with an anti-VEGFR2 antibody and anti-VEGFR-A antibody on tumor progression is not clear. In this study, we examined the anti-tumor effect of the combination treatment using BALB/c-nu/nu mouse xenograft model subcutaneously injected with human gastric cancer MKN45 cells. In this model, we evaluated intra-tumor molecular changes after the combination treatment by cDNA microarray analysis.

2021-07-28 | GSE160613 | GEO

Tumor-independent host gene expression changes induced by VEGFR2 antibody

Project description:Transcriptome analysis was used to identify tumor-independent changes after treatment with mouse VEGFR2 neutralizing antibody.

2018-03-29 | GSE112467 | GEO

Transcriptomic profiling of metastasis-associated lung endothelial cells from mice treated with anti-VEGFA antibody (B20.4.1.1)

Project description:Transcriptomic profiling of metastasis-associated lung endothelial cells from mice treated with anti-VEGFA antibody (B20.4.1.1)

| PRJNA657596 | ENA

Expression date from endothelial cells stimulated with anti-HLA class I and anti-A antibody

Project description:While donor specific antibody (DSA) against HLA class II could frequently cause chronic antibody-mediated rejection (ABMR) in organ transplantation, anti-A/B antibody would not do so, because blood group ABO-incompatible transplantation has shown favorable graft outcome. Recently, an increasing attention has been paid to the importance of direct allorecognition of CD4 T-cells against HLA-class II expressed on graft endothelial cells. However, the effect of allo-antibody binding on its allorecognition remains unclear. Microarray analysis and molecular profiling demonstrated that CD275 (PD-L1) expression was increased by anti-A/B ligation-mediated ERK inactivation in endothelial cells despite IFNγ stimulation.

2018-09-28 | GSE120545 | GEO

Single cell RNA sequencing for dental pulp cells in endothelial Vegfr2 knockout mice

Project description:Single cell RNA sequencing for dental pulp cells of first molars in control and endothelial Vegfr2 knockout mice at P12

2022-02-03 | GSE181175 | GEO

Transcriptomic profiling of metastasis-associated lung endothelial cells from mice treated with anti-VEGFA antibody (B20.4.1.1)

2021-12-31 | GSE156351 | GEO

Expression date from endothelial cells stimulated with anti-HLA class I and anti-A antibody

Project description:Expression date from endothelial cells stimulated with anti-HLA class I and anti-A antibody

| PRJNA493548 | ENA

VEGFR2

Project description:VEGFR2 Y949F mutation

| PRJEB44298 | ENA

VEGFR2 pY1173 binding partners as identified by shotgun proteomics

Project description:The main goal of the project was to identify proteins binding to vascular endothelial growth factor receptor 2 (VEGFR2) phosphorylation site Y1173. Synthetic peptides, phosphorylated or not, covering different tyrosine phosphorylation sites in VEGFR2 were immobilized and incubated with cell lysates from human umbilical vein endothelial cells. Retained proteins were analyzed by mass spectrometry. Proteins specifically binding to pY1173 peptide were categorized with regard to the presence of an Src Homology 2 (SH2) domain and the main hits were validated in intact cells treated or not with VEGF, for their ability to bind to the activated wild type VEGFR2 but not to a mutant Y1173F VEGFR2. The role of the pY1173 binding partners in VEGF-regulated endothelial biology was further examined in vitro and in vivo.

2023-09-19 | PXD041024 | Pride

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