Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Single-cell RNA-sequencing identifies anti-cancer immune phenotypes in the early lung metastatic niche during breast cancer

ABSTRACT: Single-cell RNA-sequencing identifies anti-cancer immune phenotypes in the early lung metastatic niche during breast cancer

PROVIDER: PRJNA1263479 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR33583529_1.fastq.gz	Fastqsanger.gz
	SRR33583529_2.fastq.gz	Fastqsanger.gz
	SRR33583530_1.fastq.gz	Fastqsanger.gz
	SRR33583530_2.fastq.gz	Fastqsanger.gz
	SRR33583531_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 48

Similar Datasets

Single-cell RNA-sequencing identifies anti-cancer immune phenotypes in the early lung metastatic niche during breast cancer

Project description:This experiment looks at the dissection of the microenvironment in the lung metastatic niche in a model of murine triple-negative breast cancer as disease progresses. Mice received an orthotopic inoculation of 4T1 cells and disease was allowed to progress for 7, 14, or 21 days correlating to the pre-metastatic, micro-metastatic, and metastatic niche, respectively. Healthy controls were obtained along with each time point.

2023-03-06 | E-MTAB-11741 | biostudies-arrayexpress

Single-cell RNA-sequencing identifies anti-cancer immune phenotypes in the early lung metastatic niche during breast cancer

Project description:Single-cell RNA-sequencing identifies anti-cancer immune phenotypes in the early lung metastatic niche during breast cancer

| PRJEB52769 | ENA

Single-cell RNA-sequencing identifies anti-cancer immune phenotypes in the early lung metastatic niche during breast cancer

Project description:We performed single-cell RNA sequencing (scRNA-seq) to analyze the immune microenvironment at both the natural metastatic site in the lung and a synthetic metastatic site within a biomaterial implant (scaffold) using the 4T1 murine model of metastatic triple-negative breast cancer.

2025-05-19 | GSE297298 | GEO

Single cell RNA-seq of an native and engineered metastatic niche in a metastatic breast cancer murine model

Project description:Metastatic lesions are typically not found until patients self-report symptoms or they become radiologically evident. We have developed an engineered metastatic niche (scaffold) that recruits aggressive tumor cells prior to their colonization in other organs. The engineered niche can be monitored for dynamic gene expression, and changes at this site are analogous to those in a native metastatic site (lung) for triple negative breast cancer (4T1 cells). We were able to develop a 10-gene signature from the scaffold that accurately monitors disease progression and recurrence or resistance to resection therapy. This data set acts to dissect the heterogeneity of the cell populations in the engineered and native metastatic niche and identify the cell types that contribute to the success of the signature.

2022-08-02 | E-MTAB-8503 | biostudies-arrayexpress

An Engineered Niche Delineates Metastatic Potential of Breast Cancer

Project description:We aimed to identify metastatic disease prior to the formation of an overt secondary tumor in triple-negative breast cancer using sister cell lines 4T1 (metastatic), 4T07 (invasive, non-metastatic), and 67NR (non-metastatic). We used a porous, polycaprolactone scaffold, that serves as an engineered metastatic niche, to identify metastatic disease through the changing microenvironment.

2023-11-06 | GSE233001 | GEO

An Engineered Niche Delineates Metastatic Potential of Breast Cancer

Project description:An Engineered Niche Delineates Metastatic Potential of Breast Cancer

| PRJNA974700 | ENA

A novel labelling strategy enables spatial resolution of metastatic niche cellular composition and uncovers lung stem cell activity proximal to breast cancer

Project description:Cancer cell behaviour is strongly influenced by the surrounding cellular environment, making the characterization of the local tumour microenvironment (or niche) a fundamental question in tumour biology. To date, a direct investigation of the early cellular changes induced by metastatic cells within the surrounding tissue is difficult to achieve, especially at early micro-metastatic stages and for low frequency niche populations. Here we present the strategy whereby metastatic cancer cells release a cell-penetrating fluorescent protein that is efficiently taken up by neighbouring cells, allowing spatial identification of the local metastatic cellular environment within the whole tissue. Notably, this strategy can be used to follow metastatic niches from early micro-metastasis to late macro-metastasis, allowing temporal resolution. Moreover, the presence of low represented niche cells can be detected and characterized among the bulk tissue. To highlight its potential, we have used this niche-labelling strategy to study the lung metastatic environment of breast cancer cells. We uncover the presence of lung parenchymal cells within the metastatic niche where lung epithelial cells show stem cell-like features with expression of lung progenitor markers, multi-lineage differentiation potential and self-renewal activity. Moreover, lung epithelial cells can be directly perturbed by cancer cells in ex vivo co-culture assays and support their growth. In summary, here we describe a novel labelling system that enables spatial resolution of the metastatic microenvironment and provide evidence that the tissue cellular environment surrounding metastatic growth is characterized by undifferentiated features. The data highlight the significant potential of this method as a platform for new discoveries.

2019-08-21 | PXD010597 | Pride

Bidirection activation of stem-like programs in metastatic cancer and alveolar type II cells within the niche

Project description:A key step for metastatic outgrowth involves the generation of a deeply altered microenvironment (niche) that supports the malignant behavior of cancer cells. The complexity of the metastatic niche has posed a significant challenge in elucidating the underlying programs driving its origin. Here, by focusing on early stages of breast cancer metastasis to the lung in mice, we describe a cancer-dependent chromatin remodeling and activation of developmental programs in alveolar type 2 (AT2) cells within the niche. We show that metastatic cells can prime AT2 cells into a reprogrammed multilineage state. In turn, this cancer-induced reprogramming of AT2 cells promoted stem-like features in cancer cells and enhanced their initiation capacity. In conclusion, we propose the concept of "reflected stemness" as an early phenomenon during metastatic niche initiation, wherein metastatic cells reprogram the local tissue into a stem-like state that enhances intrinsic cancer-initiating potential, creating a positive feedback loop where tumorigenic programs are amplified.

2024-05-02 | GSE240040 | GEO

Single-cell RNA-sequencing identifies anti-cancer immune phenotypes in the early lung metastatic niche during breast cancer.

Project description:Microenvironmental changes in the early metastatic niche may be exploited to identify therapeutic targets to inhibit secondary tumor formation and improve disease outcomes. We dissected the developing lung metastatic niche in a model of metastatic, triple-negative breast cancer using single-cell RNA-sequencing. Lungs were extracted from mice at 7-, 14-, or 21 days after tumor inoculation corresponding to the pre-metastatic, micro-metastatic, and metastatic niche, respectively. The progression of the metastatic niche was marked by an increase in neutrophil infiltration (5% of cells at day 0 to 81% of cells at day 21) and signaling pathways corresponding to the hallmarks of cancer. Importantly, the pre-metastatic and early metastatic niche were composed of immune cells with an anti-cancer phenotype not traditionally associated with metastatic disease. As expected, the metastatic niche exhibited pro-cancer phenotypes. The transition from anti-cancer to pro-cancer phenotypes was directly associated with neutrophil and monocyte behaviors at these time points. Predicted metabolic, transcription factor, and receptor-ligand signaling suggested that changes in the neutrophils likely induced the transitions in the other immune cells. Conditioned medium generated by cells extracted from the pre-metastatic niche successfully inhibited tumor cell proliferation and migration in vitro and the in vivo depletion of pre-metastatic neutrophils and monocytes worsened survival outcomes, thus validating the anti-cancer phenotype of the developing niche. Genes associated with the early anti-cancer response could act as biomarkers that could serve as targets for the treatment of early metastatic disease. Such therapies have the potential to revolutionize clinical outcomes in metastatic breast cancer.

| S-EPMC9643644 | biostudies-literature

Bidirection activation of stem-like programs in metastatic cancer and alveolar type II cells within the niche [RNA-seq]

Project description:A key step for metastatic outgrowth involves the generation of a deeply altered microenvironment (niche) that supports the malignant behavior of cancer cells. However, it is unclear whether a fundamental program driving the generation of this de novo cellular environment can be identified. Here, by focusing on breast cancer metastasis to the lung, we describe a cancer-dependent chromatin remodeling and activation of developmental programs in alveolar type II (AT2) cells. We have identified a relationship linking high metastatic competency in the lung with the induction of a multilineage state in AT2 cells in the niche. In turn, this cancer-induced reprogramming of AT2 cells promoted stem-like features in the cancer cells. In conclusion, we propose the concept of “reflected stemness” during metastatic niche initiation, whereby metastatic cells reprogram the local tissue into a stem-like state that enhance intrinsic cancer-initiating potential, creating a positive feedback loop where tumorigenic programs may be amplified.

2024-05-02 | GSE240037 | 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