Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene expression profile at single cell level of brain metastasis-associated astrocytes

ABSTRACT: Gene expression profile at single cell level of brain metastasis-associated astrocytes

PROVIDER: PRJNA949572 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR23991147_1.fastq.gz	Fastqsanger.gz
	SRR23991147_2.fastq.gz	Fastqsanger.gz
	SRR23991148_1.fastq.gz	Fastqsanger.gz
	SRR23991148_2.fastq.gz	Fastqsanger.gz

Items per page:

1 - 4 of 4

Similar Datasets

Gene expression profile at single cell level of brain metastasis-associated astrocytes

Project description:We used single cell RNA sequencing (scRNA-seq) to analyze the heterogeneity of astrocytes in brain metastasis

2024-08-30 | GSE228368 | GEO

Gene expression profile at single cell level of human brain metastasis samples

Project description:We used Chromium Fixed RNA Profiling to analyze the heterogeneity of astrocytes in brain metastasis at the single cell level

2024-08-30 | GSE254379 | GEO

STAT3 labels a subpopulation of reactive astrocytes required for brain metastasis

Project description:The brain microenvironment imposes a particularly intense selective pressure on metastasis initiating cells, but successful metastasis bypass this control through mechanisms that are poorly understood. Reactive astrocytes are key components of this microenvironment, as they have been observed to confine brain metastasis without infiltrating the lesion. We describe a subpopulation of reactive astrocytes surrounding metastatic lesions that are characterized by the activation of STAT3 pathway. Blocking STAT3 signaling in this subpopulation of reactive astrocytes reduces experimental brain metastasis from different primary tumor sources, even at advanced stages of colonization. We conclude that brain metastatic cells induce and maintain the co-option of a pro-metastatic program driven by STAT3 in a subpopulation of reactive astrocytes. We also show that a safe and orally bioavailable treatment that inhibits STAT3 in patients with established brain metastasis and extracranial disease exhibits significant antitumor effects, especially in the CNS where several complete responses were achieved. Given that brain metastasis imposes significant morbidity and mortality, our experimental results suggest a novel treatment for increasing survival in patients with secondary brain tumors.

2018-07-16 | PXD008956 | Pride

Type I Interferon Response in Astrocytes Promotes Brain Metastasis by Enhancing Monocytic Myeloid Cell Recruitment

Project description:Cancer metastasis to the brain is a significant clinical problem. Metastasis is the consequence of favorable interactions between invaded cancer cells and the microenvironment. Here, we demonstrate that cancer-activated astrocytes create a sustained low-level activated type I interferon (IFN) microenvironment in brain metastatic lesions. We further confirm that the IFN response in astrocytes facilitate brain metastasis. Mechanistically, IFN signaling in astrocytes activates C-C Motif Chemokine Ligand 2 (CCL2) production, which further increases the recruitment of monocytic myeloid cells. The correlation between CCL2 and monocytic myeloid cells is confirmed in clinical brain metastasis samples. Lastly, genetically or pharmacologically inhibiting C-C Motif Chemokine Receptor 2 (CCR2) significantly reduces brain metastases. Our study clarifies a pro-metastatic effect of type I IFN in the brain even though IFN response has been considered to have anti-tumor effects. Moreover, this work expands our understandings on the interactions between cancer-activated astrocytes and immune cells in brain metastasis.

2023-03-16 | GSE224302 | GEO

Gene expression profile at single cell level of human brain metastasis samples

Project description:Gene expression profile at single cell level of human brain metastasis samples

| PRJNA1070280 | ENA

Polyunsaturated Fatty Acids from Astrocytes Activates PPAR Gamma Signaling in Cancer Cells to Promote Brain Metastasis

Project description:Brain metastasis, the most ominous form of melanoma and carcinoma, is the consequence of favorable interactions between the invaded cancer cells and the brain cells. Peroxisome proliferator-activated receptor gamma (PPARɣ) has ambiguous functions in cancer development and its relevance in advanced brain metastasis remains unclear. Here, we demonstrate that astrocytes, the unique brain glia cells, activate PPARɣ in brain metastatic cancer cells. PPARɣ activation enhances cell proliferation and metastatic outgrowth in the brain. Mechanistically, astrocytes have a high content of polyunsaturated fatty acids that acts as ‘donors’ of PPARɣ activators to the invaded cancer cells. In clinical samples, PPARɣ signaling is significantly higher in brain metastatic lesions. Notably, systemic administration of PPARɣ antagonist significantly reduces brain metastatic burden in vivo. Our study clarifies a prometastatic role for PPARɣ signaling in cancer metastasis in the lipid rich brain microenvironment and argues for the use of PPARɣ blockade to treat brain metastasis.

2020-09-17 | GSE137687 | GEO

Amyloid Beta Promotes Brain Metastasis

Project description:Brain metastasis is a significant cause of morbidity and mortality in multiple cancer types and represents an unmet clinical need. The mechanisms that mediate metastatic cancer growth in the brain parenchyma are largely unknown. Melanoma, which has the highest rate of brain metastasis among common cancer types, is an ideal model to study how cancer cells adapt to the brain parenchyma. We utilized pairs of brain metastasis-derived (BM) and non-brain metastasis-derived (NBM) melanoma short term cultures (STCs) obtained from the same patient. We performed TMT based multiplexed analysis of these cell lines using off-line fractionation to increase our proteomics coverage. Our unbiased proteomics analysis of these melanoma short-term cultures revealed that proteins implicated in neurodegenerative pathologies are differentially expressed in melanoma cells explanted from brain metastases compared to those derived from extracranial metastases. We showed that melanoma cells require amyloid beta for growth and survival in the brain parenchyma. Melanoma-secreted A beta activates surrounding astrocytes to a pro-metastatic, anti-inflammatory phenotype and prevents phagocytosis of melanoma by microglia. Finally, we demonstrate that pharmacological inhibition of Abeta decreases brain metastatic burden.

2022-02-10 | MSV000088814 | MassIVE

TIMP1 mediates astrocyte-dependent local immunosuppression in brain metastasis acting on infiltrating CD8+ T cells.

Project description:Immunotherapies against brain metastases have shown clinical benefits mainly when applied to locally asymptomatic patients. It is currently unclear why responses to this therapy drop in symptomatic brain metastases, since the use of corticoids is not consistently involved. We report here that a subpopulation within STAT3+ brain metastasis-associated astrocytes is responsible to block the anti-tumor activity of infiltrating CD8+ T cells. The underlying molecular crosstalk involving astrocyte-secreted TIMP1 signaling on CD63+ CD8+ T cells proves a strong immunomodulatory role of astrocytes in the context of brain metastases. By using genetic and pharmacologic approaches applied not only to mouse models, but also to alive human brain metastases we conclude that a combined immunotherapy blocking this local immunosuppressive hub could benefit patients with symptomatic brain metastases. Furthermore, the detection of TIMP1 in the CSF provides a biomarker to select patients for this therapeutic approach. Our findings uncover the importance of dissecting the heterogeneity within the microenvironment at the functional level and the emerging cellular networks to improve the efficacy of organ-specific therapies in metastasis.

2024-08-27 | PXD040436 | Pride

Inhibition of extracellular vesicle-derived miR-146a-5p decreases the progression of melanoma brain metastasis in vitro and in vivo

Project description:Development of melanoma brain metastasis is caused by an interaction between tumor cells and normal cells in the brain microenvironment. miRNAs delivered by exosomes derived from the tumor cells seem to prime the brain microenvironment, prior to extravasation of tumor cells into the brain. We investigated miRNA in exosomes extracted from normal (astrocytes, melanocytes) and metastatic melanoma cells (brain, skin and lymph node metastasis). We have discovered that miR-146a-5p is an important player in brain metastatic development: this miRNA was highly upregulated in exosomes from melanoma brain metastasis cells, compared to normal cells.

2023-09-29 | E-MTAB-11798 | biostudies-arrayexpress

Breast cancer brain metastasis

Project description:Breast cancer brain metastasis

| PRJNA970206 | ENA