Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Immune cell infiltration into brain tumor microenvironment is mediated by Rab27-regulated vascular wall integrity

ABSTRACT: To investigate the functional role of Rab27a/b in glioblastoma. We established different roles of brain endothelial cells at physoilogical and in tumor states in the genetically mutated Rab27a/b double knock out murine tissues. We performed single cells gene expression profiling analysis using data obtained from RNA-seq from the brains of non-tumor and glioma tissues derived by injection of GL261 tumor cells in Rab27a/b dHET and Rab27a/b dKO mice.

ORGANISM(S): Mus musculus

PROVIDER: GSE268654 | GEO | 2025/04/15

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Immune cell infiltration into brain tumor microenvironment is mediated by Rab27-regulated vascular wall integrity

Project description:Immune cell infiltration into brain tumor microenvironment is mediated by Rab27-regulated vascular wall integrity

| PRJNA1118199 | ENA

Project description:Whole genome sequencing of Rab27a/b DKO mice

| PRJNA818694 | ENA

Mus musculus strain:BL57J/6

Project description:Whole genome sequencing of Rab27a/b DKO mice

| PRJNA818629 | ENA

RNASeq analysis to unravel molecular networks driving leukemia in Ebf1+/-Pax5+/- (dHet) B-ALL mice

Project description:To profile gene expression changes in Ebf1+/-Pax5+/- (dHet) leukemic mice, we performed RNASeq analysis in dHet B-ALL, dHet proB and wt proB cells.

2020-10-19 | GSE158661 | GEO

Microarray analysis to unravel molecular networks driving leukemia in Ebf1+/- Pax5+/- (dHet) B-ALL mice

Project description:To profile gene expression changes in Ebf1+/-Pax5+/- (dHet) B-ALL mice, we performed microarray analysis in dHet B-ALL, dHet proB and wt proB cells

2020-10-19 | GSE158645 | GEO

Expression data for Rab27a knockdown in the KPC 4662 pancreatic ductal adenocarcinoma cell line

Project description:Pancreatic cancer is an aggressive malignancy, often diagnosed at metastatic stages. Several studies have implicated systemic factors, such as extracellular vesicle release and myeloid cell expansion, in the establishment of pre-metastatic niches in cancer. The Rab27a GTPase is overexpressed in advanced cancers, can regulate vesicle trafficking, and has been previously linked to non-cell autonomous control of tumor growth and metastasis, however, the role of Rab27a itself in the metastatic propensity of pancreatic cancer is not well understood. Here, we have established a model to study how Rab27a directs formation of the pre-metastatic niche. Loss of Rab27a in pancreatic cancer cells did not decrease tumor growth in vivo, but resulted in altered systemic myeloid cell expansion, both in the primary tumors and at the distant organ sites. In metastasis assays, loss of Rab27a expression in tumor cells injected into circulation compromised efficient outgrowth of metastatic lesions. However, Rab27a knockdown cells had an unexpected advantage at initial steps of metastatic seeding, suggesting that Rab27a may alter cell-autonomous invasive properties of the tumor cells. Gene expression analysis of gene expression revealed that downregulation of Rab27a increased expression of genes involved in epithelial-to-mesenchymal transition pathways, consistent with our findings that primary tumors arising from Rab27a knockdown cells were more invasive. Overall, these data reveal that Rab27a can play divergent roles in regulating pro-metastatic propensity of pancreatic cancer cells: by generating pro-metastatic environment at the distant organ sites, and by suppressing invasive properties of the cancer cells.

2020-04-16 | GSE148439 | GEO

Cancer-cell-secreted miR-9-5p regulates cholesterol homeostasis to promote tumor metastasis [TF TB Rab27AKD miR-9KO]

Project description:To investigate the effects of breast cancer derived EVs on liver metabolism,we inoculated MDA-MB-231,231 /Rab27A KD and 231 /miR-9 KO cells into subcutaneous tumor in NSG mice. We then performed gene expression profiling analysis using data obtained from RNA-seq of liver from mice xenografted MDA-MB-231 cells (tumor bearing) or MDA-MB-231/Rab27A KD cells (231/Rab27A KD) or MDA-MB-231 /miR-9 KO (231/miR-9 KO) and tumor free mice.

2024-08-31 | GSE222707 | GEO

ATACSeq and genome-wide binding profile of EBF1 and Pax5 to unravel molecular networks driving leukemia in Ebf1+/-Pax5+/- (dHet) B-ALL mice.

Project description:ATACSeq, EBF1 ChIPSeq and Pax5 ChIPSeq of dHet B-ALL, dHet proB and wt proB cells.

2020-10-19 | GSE158671 | GEO

Single-nucleus RNA-sequencing (snRNA-Seq) of brain cells from tumor-bearing C57BL/6 mice

Project description:GL261-derived glioblastoma stem cells (GSCs) form aggressive tumors when implanted into the brains of C57BL/6 mice. We used snRNA-Seq to analyze GL261 and GL261-GSCs as well as tumor samples of 7 and 28 days of development.

2024-03-28 | GSE246154 | GEO

RNA-seq analysis of immunogenic actions of metronomic cyclophosphamide treatment: dependence of gene responses on tumor model, mouse host, and drug schedule

Project description:RNA-seq analysis was performed using RNA isolated from three tumor models (GL261 glioma, LLC Lewis lung carcinoma, B16F10 melanoma) implanted subcutaneousy in C57BL/6 mice, or in ICR scid mice. Mice were untreated or were treated with cyclophosphamide (CPA) given on a 6-day repeating metronomic schedule (CPA/6d), except as noted. Results from these global transcriptome analysis indicated substantial elevation of basal GL261 immune infiltration and strong activation by CPA/6d treatment of GL261 immune stimulatory pathways and their upstream regulators, but without preferential depletion of negative immune regulators compared to LLC and B16F10 tumors. In LLC tumors, where CPA/6d treatment was found to be anti-angiogenic, CPA/6d suppressed VEGFA target genes and down regulated cell adhesion and leukocyte transendothelial migration genes. In GL261 tumors implanted in adaptive immune-deficient scid mice, where CPA/6d-induced GL261 regression is incomplete and late tumor growth rebound can occur, T cell receptor signaling and certain cytokine-cytokine receptor responses seen in B6 mice were deficient. Extending the CPA treatment interval from 6 to 9 days (CPA/9d) â which results in a strong but transient natural killer cell response followed by early tumor growth rebound â induced fewer cytokines and increased expression of drug metabolism genes. Taken together, these findings elucidate molecular response pathways activated by intermittent metronomic CPA treatment and identify deficiencies that characterize immune-unresponsive tumor models and drug schedules. RNA isolated from various tumor cell lines implanted s.c in C57BL/6 mice or scid mice, untreated or treated with cyclophosphamide (CPA) given on a metronomic schedule, were prepared and used for stranded or unstranded RNA-seq.

2016-08-01 | E-GEOD-71491 | biostudies-arrayexpress

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