Distinctive properties of endothelial cells from tumor and normal tissue in human breast cancer
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA744083 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR15048891.fastq.gz | Fastqsanger.gz | |||
| SRR15048892.fastq.gz | Fastqsanger.gz | |||
| SRR15048893.fastq.gz | Fastqsanger.gz | |||
| SRR15048894.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 4 of 4 |
Similar Datasets
Project description:Tumor microenvironment shapes aggressiveness and is largely maintained by the conditions of angiogenesis formation. Thus endothelial cells (ECs) biological reactions are crucial to know and control the design of efficient therapies. Here we used a model of ECs representative for the breast cancer tumor site and the same but healthy organ. Cells characterization was performed at the transcriptome, protein expression levels and assessment of their functional biological responses: angiogenesis and permeability. We showed that the expression of proteins specific for ECs (ACE+, VWF+), their differentiation (CD31+, CD 133+, CD105+, CD34-), adhesion properties (ICAM-1+, VCAM-1+, CD62-L+), barrier formation (ZO-1+) were down-regulated in tumor-derived ECs. The NGS-based differential transcriptome analysis confirmed CD31-lowered expression and pointed to the increase of Ephrin-B2 and SNCAIP indicative for dedifferentiation. Functional assays confirmed these differences as angiogenesis was impaired while permeability increased in tumor-derived ECs, further validated by the distinct enhanced VEGF production in response to hypoxia, reflecting the tumor conditions. This work shows that endothelial cells differ highly significantly, both phenotypically and functionally in the tumor site vs. the normal corresponding tissue, influencing the tumor microenvironment.
2022-07-05 | GSE179509 | GEO
Project description:Tumor microenvironments shape aggressiveness and are largely maintained by the conditions of angiogenesis formation. Thus, endothelial cells' (ECs) biological reactions are crucial to understand and control the design of efficient therapies. In this work, we used models of ECs to represent a breast cancer tumor site as well as the same, healthy tissue. Cells characterization was performed at the transcriptome and protein expression levels, and the cells functional biological responses (angiogenesis and permeability) were assessed. We showed that the expression of proteins specific to ECs (ACE+, VWF+), their differentiation (CD31+, CD 133+, CD105+, CD34-), their adhesion properties (ICAM-1+, VCAM-1+, CD62-L+), and their barrier formation (ZO-1+) were all downregulated in tumor-derived ECs. NGS-based differential transcriptome analysis confirmed CD31-lowered expression and pointed to the increase of Ephrin-B2 and SNCAIP, indicative of dedifferentiation. Functional assays confirmed these differences; angiogenesis was impaired while permeability increased in tumor-derived ECs, as further validated by the distinctly enhanced VEGF production in response to hypoxia, reflecting the tumor conditions. This work showed that endothelial cells differed highly significantly, both phenotypically and functionally, in the tumor site as compared to the normal corresponding tissue, thus influencing the tumor microenvironment.
| S-EPMC8396343 | biostudies-literature
Project description:Identification of genes differentially expressed in gastric cancer endothelial cells compared to normal tissue endothelial cells.
2009-02-04 | E-TABM-424 | biostudies-arrayexpress
Project description:MeRIP sequencing reveals angiogenic properties of vascular endothelial cells
| PRJNA596787 | ENA
Project description:Interactions of cancer cells with the vasculature are essential for tumor growth and likely promote metastatic progression. Endothelial cell content and lympho-vascular invasion are generally associated with tumor aggressiveness, however, these features are generally not employed in the clinic. We aimed to determine if endothelial cell gene expression signatures could be utilized to better characterize breast tumor biology, and to establish if vascular cell-derived signatures could provide information to predict tumors likely to metastasize. Here we report on the identification of a gene signature for vascular endothelial cells, and a second for cancer-activated vasculature. Both signatures independently identify subsets of aggressive breast cancers. Interestingly, the vascular content signature and a previously identified hypoxia signature both provide prognostic information beyond currently utilized clinical parameters and intrinsic subtype classifications. In these studies, we also examined the relationship that the breast cancer subtypes have with vascular gene expression profiles, and found that claudin-low tumors and cell lines express vascular gene expression profiles and displayed endothelial-like tube formation when grown in three-dimensions. These findings are directly applicable to clinical care and therapeutic treatment design as they identify highly aggressive subsets of tumors with genetic and morphologic vascular properties. reference x sample
2014-01-01 | E-GEOD-37145 | biostudies-arrayexpress
Project description:Bulk cancer cell populations are known to display distinct metabolic properties compared to their normal counterparts. However, relatively little is known about heterogeneity of metabolic properties within tumors. In this study we show that, analogous to some normal stem cells, breast tumor initiating cells (TICs, also called cancer stem cells) have distinct metabolic properties compared to non-tumorigenic cancer cells (NTCs). Transcriptome profiling using RNA-Seq revealed TICs under-express genes involved in mitochondrial oxidative phosphorylation and although TICs are relatively quiescent, they preferentially perform glycolysis over oxidative phosphorylation compared to NTCs. TICs contain fewer mitochondria and display lower expression and activity of pyruvate dehydrogenase (Pdh), a key regulator of oxidative phosphorylation. Metabolic reprogramming of TICs by pharmacologic activation of Pdh preferentially eliminates TICs in vitro and in vivo. Our findings reveal unique metabolic properties of TICs and indicate that metabolic reprogramming represents a promising strategy for targeting these cells. Examination transcriptome profiles for breast tumor initiating cells (TICs) and non-tumorigenic cells (NTCs)
2014-07-31 | E-GEOD-41286 | biostudies-arrayexpress
Project description:High IRF1 expression endows classical PDAC cells with distinctive properties and metabolic programs (ChIP-Seq 2)
| PRJNA742000 | ENA
Project description:Bulk cancer cell populations are known to display distinct metabolic properties compared to their normal counterparts. However, relatively little is known about heterogeneity of metabolic properties within tumors. In this study we show that, analogous to some normal stem cells, breast tumor initiating cells (TICs, also called cancer stem cells) have distinct metabolic properties compared to non-tumorigenic cancer cells (NTCs). Transcriptome profiling using RNA-Seq revealed TICs under-express genes involved in mitochondrial oxidative phosphorylation and although TICs are relatively quiescent, they preferentially perform glycolysis over oxidative phosphorylation compared to NTCs. TICs contain fewer mitochondria and display lower expression and activity of pyruvate dehydrogenase (Pdh), a key regulator of oxidative phosphorylation. Metabolic reprogramming of TICs by pharmacologic activation of Pdh preferentially eliminates TICs in vitro and in vivo. Our findings reveal unique metabolic properties of TICs and indicate that metabolic reprogramming represents a promising strategy for targeting these cells.
2014-07-31 | GSE41286 | GEO
Project description:With poor prognosis and low-survival rates, Triple Negative Breast Cancer (TNBC) has been associated with increased angiogenesis, which is known to aid tumour growth and metastasis. Anti-angiogenic therapies that were developed to address this have mostly generated disappointing clinical results. Further research into targeted approaches is limited by the lack of understanding of molecular profile of cancer-associated vasculature. Here, we have applied unbiased whole transcriptome spatial profiling of in situ gene expressions of endothelial cells localized in full-face patient TNBC tissues and adjacent normal breast tissues. Our comparative analysis showed that 2412 genes were differentially expressed (padj<0.05) between the tumour endothelial cells and normal adjacent endothelial cells. Pathway enrichment showed the enrichment of gene sets related to cell-cell, cell-ECM adhesion, chromatin organization and remodeling, and protein-DNA complex subunit organization. Overall, the results have revealed unique molecular profiles and signalling pathways of tumour vasculature which can potentially enable the detection of potential targets for TNBC prognosis and anti-angiogenic treatments and provide a greater understanding of metastasis . The results of this pilot study need validation in larger independent cohorts.
2023-12-06 | GSE235640 | GEO
Project description:Comparison of C57BL/6J 8-10 weeks male mouse liver sinusoidal endothelial cells (LSEC) from normal liver and from liver injured by carbon tetrachloride administration. Keywords: other
2004-10-01 | GSE1689 | GEO