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Transcriptional regulation of Sox17 in HUVEC

ABSTRACT: We identified Sox17 as a novel angiogenic transcription factor in the context of tumor. Our data revealed that Sox17 promotes tumor angiogenesis and tumor vessel abnormality. We found that Sox17 is specifically expressed in tumor endothelial cells within tumors. Our study elucidates a novel transcriptional regulation for tumor angiogenesis

ORGANISM(S): Homo sapiens

PROVIDER: GSE37395 | GEO | 2012/12/17

SECONDARY ACCESSION(S): PRJNA159891

REPOSITORIES: GEO

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Transcriptional regulation of Sox17 in HUVEC

Project description:We identified Sox17 as a novel angiogenic transcription factor in the context of tumor. Our data revealed that Sox17 promotes tumor angiogenesis and tumor vessel abnormality. We found that Sox17 is specifically expressed in tumor endothelial cells within tumors. Our study elucidates a novel transcriptional regulation for tumor angiogenesis Control HUVECs vs. Sox17 knockdown HUVECs. Biological replicates: 3 control replicates, 3 transfected replicates.

2012-12-17 | E-GEOD-37395 | biostudies-arrayexpress

HUVEC gene profile after Sox7/Sox17 siRNA silencing

Project description:To find out the target of transcription factor Sox7 and Sox17, DNA microarray analysis was performed with RNA from Sox7 and Sox17 knockdown HUVECs.

2016-11-23 | GSE75380 | GEO

RNA analysis of Sox7- and Sox17-deficient mouse endothelial cells from high grade glioma

Project description:Glioblastoma multiforme (GBM) is a highly aggressive and vascularized malignant brain tumor. SoxF transcription factors consisting of Sox7, Sox17, and Sox18 are expressed specifically in endothelial cells (ECs) and contribute to vascular morphogenesis. While the role of Sox17 was found in subcutaneous ectopic tumors, Sox7 has not been studied in the context of tumor angiogenesis. Here, we investigated gene expression profile of RNA analysis of Sox7- and Sox17-deficient mouse endothelial cells from high grade glioma using RNA sequencing to validate molecular characteristics of Sox7 and Sox17 in high grade glioma.

2018-01-27 | GSE107530 | GEO

Cancer associated fibroblast-derived WNT2 increases tumor angiogenesis in colon cancer

Project description:WNT2 is important for placenta vascularization and acts as a pro-angiogenic factor for liver and other endothelial cells (ECs). WNT2 induction has been shown in many carcinomas and is associated with tumor progression. In colorectal cancer (CRC) WNT2 is selectively elevated in cancer associated fibroblasts (CAFs), leading to increased invasion and metastasis. However, if there is a role for WNT2 in colon cancer angiogenesis has not been addressed so far. Here, we demonstrate that WNT2 enhances EC migration and invasion, while it induces ß catenin dependent signaling in only a small subset of HUVECs. We show that siRNA-mediated knockdown of WNT2 in CAFs reduced the growth of vessel-like structures significantly in a co-culture assay, while the overexpression of WNT2 in skin fibroblasts otherwise being devoid of WNT2 led to increased angiogenesis in vitro. In a xenograft model, overexpression of WNT2 in HCT116 led to enhanced tumor volume and vessel density. Moreover, WNT2 expression correlates with vessel markers in human CRC. Secretome profiling of CAFs revealed that proteins related to angiogenesis and extracellular matrix (ECM) remodeling are regulated by WNT2. Thus, stroma-derived WNT2 positively affects angiogenesis in CRC by shifting the balance towards pro-angiogenic signals.

2020-05-26 | PXD014019 | Pride

Single cell transcriptomics profiling of vessel co-option

Project description:Vessel co-option is an alternative mode of tumor vascularization, which contributes to resistance to anti-angiogenic therapy (AAT). In contrast to vessel sprouting (angiogenesis), knowledge about the mechanisms underlying vessel co-option is minimal, precluding therapeutic strategies. We therefore single-cell RNA-sequenced 31,964 cells from a murine lung metastasis model with vessel co-option, characterized by resistance to AAT. Unexpectedly, co-opted endothelial cells (ECs) were transcriptomically indistinguishable from healthy ECs and lacked an activation signature, while co-opted pericytes expressed a quiescence signature, in contrast to activated pericytes during angiogenesis. Compared with cancer cells during angiogenesis, co-opting cancer cells were phenotypically more diverse and enriched in invasive subpopulations. Together, these data reveal new insight into vessel co-option, with possible implications for the development of therapeutic targets.

2021-06-15 | E-MTAB-9227 | biostudies-arrayexpress

Effects of the Sox17 ∆50 mutation on SOX17 function in mouse embryonic liver development

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Alternative splicing changes promoted by NOVA2 upregulation in endothelial cells and relevance for gastric cancer

Project description:Angiogenesis is crucial for cancer progression and anti-angiogenic drugs are in use for its treatment. However, their clinical benefits are unsatisfactory. Thus, a deeper understanding of the mechanisms sustaining cancer vessel growth is crucial to identify better biomarkers and novel therapeutic targets. Alternative Splicing (AS) is an essential modifier of human proteome diversity. Nevertheless, its contribution to tumor vasculature development is poorly known. NOVA2 is an important AS regulator of angiogenesis and vascular development and it is up-regulated in tumor endothelial cells (ECs) of different cancers, thus representing a potential driver of tumor blood vessels aberrancies. Here, we identified novel AS transcripts generated upon NOVA2 upregulation in ECs, suggesting a pervasive role of NOVA2 in vascular biology. In addition, we report that NOVA2 is also upregulated in ECs of gastric cancer (GC), with its expression correlating with poor overall survival of the GC patients. We also found that the AS of the newly identified NOVA2 target RapGEF6 is altered in GC patients and associated with NOVA2 expression, tumor angiogenesis and poor patient outcome. Our findings provide a better understanding of GC biology and suggest that AS might represent a potential source of biomarkers and therapeutics for novel anti-angiogenic GC treatments.

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Gene expression profiling of the tumor angiogenic switch in Rip1Tag2 mice

Project description:Angiogenesis represents a rate-limiting step during tumor progression. Molecular mechanisms driving tumor angiogenesis (e.g. implicating signaling by VEGFs and their receptors) have been elucidated and allowed to design targeted therapies. However, limits of such anti-angiogenic therapies have emerged, notably because tumor cells adapt and tumors recur in more aggressive fashions. There is therefore a need to identify novel mechanisms implicated in tumor angiogenesis that have a potential towards translational applications. Using a transgenic murine model of pancreatic neuroendocrine cancer (Hanahan, Nature 315, 1985) where angiogenesis represents an early and discrete step of multi-stage tumor progression (Folkman et al. , Nature 339, 1989), we compared non-angiogenic and angiogenic early tumors to obtain a comprehensive description of the tumor angiogenic switch at the level of gene expression.

2015-01-01 | GSE51637 | GEO

Effects of the Sox17∆50/GFP mutation on SOX17 function in mouse embryonic liver development

Project description:To determine the role of specific cis-regulatory elements within the Sox17 endoderm-preferential TSS2 promoter, we generated Sox17∆50 mutant animals, crossed them to a Sox17GFPCre (a Sox17 null allele), and surveyed how this mutation affected Sox17 expression. Livers were isolated from E12.5 Sox17∆50/GFPCRe compound heterozygous and Sox17+/+ embryos (n = 4 of each genotype), RNA isolated, and bulk RNA-Seq performed.

2024-10-31 | E-MTAB-13983 | biostudies-arrayexpress

Effects of the Sox17∆50 mutation on SOX17 function in mouse embryonic biliary development

Project description:To determine the role of specific cis-regulatory elements within the Sox17 endoderm-preferential TSS2 promoter, we generated Sox17∆50 mutant animals and surveyed how this mutation altered Sox17 expression. EPCAM+/CXCR4+ endodermal cells were isolated from E10.5 Sox17∆50/∆50 and Sox17+/+ embryos (n = 1 of each genotype). Posterior foregut and midgut regions of embryos were dissected by removal of embryonic head, heart, tail, limb buds, posterior and dorsal body trunk. Sox17+/+ and Sox17Δ50/Δ50 cell samples were labelled with barcodes from 3'CellPlex Kit (10X Genomics) and subsequently pooled together for single isolation, library preparation and sequencing.

2024-10-31 | E-MTAB-14000 | biostudies-arrayexpress

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