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An Engineered Niche Delineates Metastatic Potential of Breast Cancer

ABSTRACT: An Engineered Niche Delineates Metastatic Potential of Breast Cancer

PROVIDER: PRJNA974700 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24678000.fastq.gz	Fastqsanger.gz
	SRR24678001.fastq.gz	Fastqsanger.gz
	SRR24678002.fastq.gz	Fastqsanger.gz
	SRR24678003.fastq.gz	Fastqsanger.gz
	SRR24678004.fastq.gz	Fastqsanger.gz

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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

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 model of metastatic colonization of human bone marrow reveals breast cancer cell remodeling of the hematopoietic niche

Project description:Incomplete understanding of metastatic disease mechanisms continues to hinder effective treatment of cancer. Despite remarkable advancements toward the identification of druggable targets, treatment options for patients in remission following primary tumor resection remain limited. Bioengineered human tissue models of metastatic sites capable of recreating the physiologically relevant milieu of metastatic colonization may strengthen our grasp of cancer progression and contribute to the development of effective therapeutic strategies. We report the use of an engineered tissue model of human bone marrow (eBM) to identify microenvironmental cues regulating cancer cell proliferation and to investigate how triple-negative breast cancer cell lines influence hematopoiesis. Notably, individual stromal components of the BM niche (osteoblasts, endothelial cells, and mesenchymal stem/stromal cells) were each critical for regulating tumor cell quiescence and proliferation in the three-dimensional eBM niche. In this data set, we provide transcriptomic information from bulk RNA sequencing of MDA-MB-231 cancer cells that were pre-conditioned by being co-cultured on variations of eBM tissues. We envision that this human tissue model will facilitate studies of niche-specific metastatic progression and individualized responses to treatment.

2024-09-23 | GSE277786 | GEO

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

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

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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

Genetically engineered endothelial niche induces vascularization in human kidney organoids

Project description:Here we developed a method to incorporate a genetically engineered endothelial niche into an established protocol for generating human kidney organoids.

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Hepatocytes direct the formation of a pro-metastatic niche in the liver.

Project description:The liver is the most common site of metastatic disease in gastrointestinal malignancies, including pancreatic ductal adenocarcinoma (PDAC). While this metastatic tropism may reflect mechanical trapping of tumor cells that enter the circulation, liver metastasis is also dependent, at least in part, on the formation of a “pro-metastatic” niche that supports tumor cell seeding and colonization in the liver. However, mechanisms that orchestrate the establishment of this niche are poorly understood. Here, we show that hepatocytes coordinate accumulation of myeloid cells and fibrosis within the liver, the two defining features of a pro-metastatic niche. Early during pancreatic tumorigenesis in mice, hepatocytes demonstrate activation of Signal Transducer and Activator of Transcription 3 (STAT3) signaling and increased production of serum amyloid A1 and A2 (SAA). Overexpression of SAA by hepatocytes also occurs in PDAC patients with liver metastases, and many patients with locally advanced and metastatic disease display elevated levels of circulating SAA. STAT3 activation in hepatocytes and the subsequent production of SAA are dependent on interleukin 6 (IL-6) that is released into the circulation by non-malignant cells that reside adjacent to malignant cells in the pancreas. Genetic ablation or blockade of components of IL-6/STAT3/SAA signaling in hepatocytes effectively prevents the establishment of a pro-metastatic niche and inhibits metastatic seeding in the liver. Collectively, our data reveal an intercellular network underpinned by hepatocytes that forms the basis for a pro-metastatic niche in the liver and identify new therapeutic targets for pancreatic cancer.

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