Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Role of EGR1 in vasculogenic mimicry of MDA-MB-231 cells

ABSTRACT: Vasculogenic mimicry (VM) is an intriguing phenomenon observed in tumor masses, in which cancer cells organize themselves into capillary-like channels that closely resemble the structure and function of blood vessels. Although VM is believed to contribute to alternative tumor vascularization, the detailed regulatory mechanisms controlling these cellular processes remain poorly understood. Our study aimed to investigate the role of Early Growth Response 1 (EGR1) in regulating VM in aggressive cancer cells, specifically MDA-MB-231 triple-negative breast cancer cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE240489 | GEO | 2023/08/15

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Gene expression of osteosarcama cell line with vasculogenic mimicry phenotype

Project description:Vasculogenic mimicry has been generally accepted as a new form of tumor vascularization and regarded as an unfavorable prognostic factor in multiple aggressive malignancies. We previously reported the presence of vasculogenic mimicry in osteosarcoma patients. The mechanistic basis for osteosarcoma VM remains unclear. We used microarrays to detail the global programme of gene expression between 143B cells and HOS cells exposed to Matrigel which showed greatly different vasculogenic mimicry formation potential and identified distinct classes of vasculogenic mimicry-realted genes during this process.

2018-09-15 | GSE119975 | GEO

Proteomics analysis on COE inhibiting vasculogenic mimicry in hepatocellular carcinoma

Project description:New strategies and drugs are urgently needed to improve the treatment of hepatocellular carcinoma (HCC). Vasculogenic mimicry (VM) has been elucidated being associated with the progression of HCC and anti-VM could be a promising strategy. Celastrus orbiculatus extract (COE), a mixture of 11 terpenoids isolated from the Chinese Herb Celastrus Orbiculatus Vine, has been elucidated to be able to disrupt VM formation in HCC. This study aims to dissect and identify the potential targets of COE on anti-VM formation both in vitro and in vivo that are distinct from our previous study. Proteomics analysis was used to identify differential proteins in HCC cells treated with or without COE. Cells invasion was examined using Transwell. Matrigel was used to establish a 3-D culture condition for VM formation in vitro. RT-PCR and Western Blot were used to examine changes of mRNA and protein respectively. Clinical resected samples were applied to confirm association between VM formation and identified targets. Subcutaneous xenograft tumor model was established to observe tumor growth and VM formation in vivo. PAS-CD34 dual staining was used to detect VM in vivo. A total of 194 proteins were identified to be differentially expressed in HCC cells treated with or without COE. In the 93 down-regulated proteins EphA2 stood out to be regulated on both RNA and protein level. Disruption EphA2 using COE or NVP inhibited VM formation and decreased VM associated biomarkers. In xenograft mouse model, COE inhibited tumor growth and VM formation via down-regulating EphA2. Taken together, our results indicate that COE could be used in HCC treatment because of its promising anti-VM effect.

2021-05-03 | PXD022203 | Pride

EBV-induced CXCL8 upregulation promotes vasculogenic mimicry in gastric carcinoma via NF-κB signaling

Project description:Epstein-Barr virus (EBV)-associated gastric carcinoma (EBVaGC) is a distinct entity that has conspicuously tumor microenvironment compared with EBV-negative gastric carcinoma. However, the exact role of EBV in gastric carcinogenesis remains elusive. In the present study, we found that EBV upregulated CXCL8 expression, and CXCL8 significantly promoted vasculogenic mimicry (VM) formation of gastric carcinoma cells. In accordance with these observations, CXCL8 increased cell proliferation and migration of AGS and BGC823 cells, respectively. In addition, activation of NF-κB signaling was involved in VM formation induced by CXCL8, which was blocked by NF-κB inhibitor BAY 11-7082. Furthermore, EBV encoded lncRNA RPMS1 activated the NF-κB signaling cascade, which is responsible for EBV-induced VM formation. Both xenografts and clinical samples of EBVaGC exhibit VM histologically, which are correlated with CXCL8 over-expression. Finally, CXCL8 is positively correlated with overall survival in gastric carcinoma patients. In conclusion, EBV-upregulated CXCL8 expression promotes VM formation in gastric carcinoma via NF-κB signaling and CXCL8 may serve as a novel anti-tumor target for EBVaGC.

2021-10-14 | GSE185627 | GEO

Single cell RNA-seq of 4T1-T vasculogenic mimicry-competent mammary tumors

Project description:We have previously described a sub-clones of the 4T1 mammary carcinoma cell line that are proficient for vasculogenic mimciry (VM), namely 4T1-E and 4T1-T. In vitro assays suggest that not all cells within these lines a VM-competent. To explore subsets of cells within tumors derived from these cells that may display VM properties we utilized single cell RNA-Seq of 4T1-T mammary fat-pad tumors.

2023-07-26 | GSE230642 | GEO

An interplay between extracellular matrix proteins and the cancer cell promotes the multistep process of in vitro vasculogenic mimicry formation.

Project description:Cancer vasculogenic mimicry (VM) is the formation of vasculature structures in the absence of endothelial cells. We previously established an in vitro model that facilitates the formation of a lumen-containing and fluid-conducting tubular structures after 4 days cancer cell growth on Matrigel. Herein, we mechanistically characterize this model in breast and ovarian cancer cell lines demonstrating distinct phases of VM formation and the dependence of specific extracellular matrix proteins. We report that VM occurs in four distinct stages. Firstly, alignment, migration then clustering delineate the area of the future tubular structure. Secondly, contraction of aligned structures followed by loss of attachment of some cells and cellular blebbing. Thirdly, a phase of mass proliferation followed by the raising of specific areas of the cancer cell mass above the Matrigel (bridge). Finally, the formation of a cell monolayer closes the tubular structure, forms a glycoprotein-rich luminal lining, then elevates the structure. Only later stages of VM require AKT and FAK signaling. We demonstrate that the lining of the tubular lumen is rich in laminin. Laminin 111 (but not collagen I) must be presence in the extracellular matrix (Matrigel) for VM to occur and integrin β1, but not integrin β3, is required. RNASeq demonstrates that formation is principally post-transcriptional regulation, however, this technique together with siRNA knockdown identified the first and essential biological function for the protein SMIM11A. VM is associated with poor patient survival and thus an understanding of the mechanism of VM may bring to light novel anticancer targets.

2024-04-11 | GSE263232 | GEO

Antibody-drug conjugate αEGFR-E-P125A reduces triple-negative breast cancer vasculogenic mimicry, motility, and metastasis through inhibition of EGFR, integrin, and FAK/STAT3 signaling

Project description:Primary tumor growth and metastasis in triple-negative breast cancer (TNBC) require supporting vasculature, which develop through a combination of endothelial angiogenesis and vasculogenic mimicry (VM), a process associated with aggressive metastatic behavior in which vascular-like structures are lined by tumor cells. We developed αEGFR-E-P125A, an antibody-endostatin fusion protein that delivers a dimeric, mutant endostatin (E-P125A) payload that inhibits TNBC angiogenesis and VM in vitro and in vivo. To characterize the mechanisms associated with induction and inhibition of VM, RNA-seq of MDA-MB-231-4175 TNBC cells grown in a monolayer (2D) was compared to cells plated on Matrigel undergoing VM (3D). We then compared RNA-seq between TNBC cells in 3D and cells in 3D with VM inhibited by αEGFR-E-P125A (αEGFR-E-P125A). Gene set enrichment analysis (GSEA) demonstrated that VM induction activated the IL6-JAK-STAT3 and angiogenesis pathways, which were downregulated by αEGFR-E-P125A treatment. Correlative analysis of the phospho-proteome demonstrated decreased EGFR phosphorylation at Y1069, along with decreased phosphorylation of focal adhesion kinase (FAK) Y397 and STAT3 Y705 sites downstream of α5β1 integrin. Suppression of phosphorylation events downstream of EGFR and α5β1 integrin demonstrated that αEGFR-E-P125A interferes with ligand-receptor activation, inhibits VM, and overcomes oncogenic signaling associated with EGFR and α5β1 integrin crosstalk. In vivo, αEGFR-E-P125A treatment decreased primary tumor growth and VM, reduced lung metastasis, and confirmed the inhibition of signaling events observed in vitro. Simultaneous inhibition of EGFR and α5β1 integrin signaling by αEGFR-E-P125A is a promising strategy for the inhibition of VM, tumor growth, motility, and metastasis in TNBC and other EGFR-overexpressing tumors.

2024-01-29 | GSE253789 | GEO

Gene expression profiling of neuroendocrine (NE) and non-neuroendocrine (non-NE) cells derived from ex vivo cultures of small cell lung cancer (SCLC) circulating tumour cell-derived explant (CDX) model

Project description:To determine molecular processes in vasculogenic mimicry (VM) competent human SCLC CDX, we profiled gene expression by RNA sequencing in separated NE (VM deficient) and non-NE (VM competent) cells from four CDX cultured on plastic or on Matrigel.

2023-10-23 | GSE240789 | GEO

In vitro priming of human mesenchymal stromal/stem cells into 3D capillary-like structures : Implication of the Src/JAK/STAT3 signaling pathway in vasculogenic mimicry

Project description:Background: Mesenchymal stromal/stem cells (MSC) can enhance the neovascularization processes required for wound healing and are widely used as an autologous source of progenitor cells in stem cell-based therapies. However, incomplete MSC differentiation towards a vascular endothelial cell phenotype questions their involvement in an alternative process to angiogenesis, namely vasculogenic mimicry (VM), and the signal transducing events that regulate their in vitro priming into 3D capillary-like structures. Methods: Human MSC were primed on top of Cultrex matrix in order to recapitulate an in vitro 3D phenotype of VM. Total RNA was extracted, and differential gene expression assessed through RNA-Seq analysis and RT-qPCR. Transient gene silencing was achieved using specific siRNA. AG490, Tofacitinib, and PP2 pharmacological effects on VM 3D structures were analyzed using the Wimasis software. Results: In vitro VM occurred within 4 hours and was prevented by the JAK/STAT3 inhibitors AG490 and Tofacitinib, as well as by the Src inhibitor PP2. RNA-Seq highlighted STAT3 as a signaling hub contributing to VM when transcripts from 3D cultures were compared to those from 2D monolayers. Concomitant increases in IL6, IL1b, CSF1, CSF2, STAT3, FOXC2, RPSA, FN1, and SNAI1 transcript levels suggest the acquisition of a combined angiogenic, inflammatory and epithelial-to-mesenchymal transition phenotype in 3D cultures. Increases in STAT3, FOXC2, RPSA, Fibronectin, and Snail protein expression were confirmed in 3D cultures. STAT3 and RPSA gene silencing abrogated in vitro VM. Conclusions: In vitro VM priming of MSC into 3D structures requires Src/JAK/STAT3 signaling. This molecular evidence supports a clinically feasible MSC-mediated pseudo-vasculature process that could temporarily sustain grafts through VM until the host vasculature is able to infiltrate and remodel injured tissues.

2024-05-14 | GSE267328 | GEO

Gene expression of osteosarcama cell line with vasculogenic mimicry phenotype

Project description:Gene expression of osteosarcama cell line with vasculogenic mimicry phenotype

| PRJNA490884 | ENA

Next Generation Sequencing Facilitates Quantitative Analysis of FZD2 Knockdown/Control SNU449 Cell Line Transcriptomes

Project description:We report evidence that FZD2 is a driver for EMT, cancer stem cell (CSC) property, and vasculogenic mimicry (VM) in hepatocellular carcinoma. To further examine the transcriptional changes in response to FZD2 depletion, we performed RNA-seq with FZD2 knockdown and control SNU449 cells by BGISEQ-500.

2020-12-31 | GSE112363 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data