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Metastatic medulloblastoma remodels the local leptomeningeal microenvironment to promote further metastatic colonization and growth

ABSTRACT: Metastatic medulloblastoma remodels the local leptomeningeal microenvironment to promote further metastatic colonization and growth

PROVIDER: PRJNA1101974 | ENA |

REPOSITORIES: ENA

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	SRR28736410.fastq.gz	Fastqsanger.gz
	SRR28736415.fastq.gz	Fastqsanger.gz

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Metastatic medulloblastoma remodels the local leptomeningeal microenvironment to promote further metastatic colonization and growth

Project description:Medulloblastoma metastasis often occurs in the leptomeningeal spaces; however, the biology of the metastatic tumour cells and the local leptomeningeal niche are poorly characterized. We performed single-cell RNA sequencing to analyze the leptomeningeal metastatic niche in a medulloblastoma mouse model.

2025-03-14 | GSE264326 | GEO

Chromatin accessibility profiling of freshly isolated mouse lung cancer LLC- and breast cancer 4T1- derived leptomeningeal metastatic cancer cells from different anatomical locations [ATAC-Seq]

Project description:Cancer cells metastatic to the leptomeninges encounter a metabolically-challenging extreme microenvironment. To understand adaptations to this space, we subjected leptomeningeal-metastatic (LeptoM) mouse breast and lung cancers isolated from either the leptomeninges or orthotopic primary sites to ATAC- and RNA-sequencing. When inhabiting the leptomeninges, the LeptoM cells demonstrated transcription downstream of retinoid-X-receptors (RXRs). We found evidence of local retinoic acid (RA) generation in both human leptomeningeal metastasis and mouse models in the form of elevated spinal fluid retinol and expression of RA-generating dehydrogenases within the leptomeningeal microenvironment. Stimulating LeptoM cells with 9-cis RA induced expression of transcripts encoding de novo fatty acid synthesis pathway enzymes in vitro. In vivo, whereas knockout of Stra6 did not alter cancer cell leptomeningeal growth, knockout of Rxra/b/g interrupted cancer cell lipid biosynthesis and arrested cancer growth. These observations illustrate a mechanism whereby locally-generated developmental cues metabolically reprogram metastatic cancer cells and suggest novel therapeutic approaches.

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Transcriptomic profiling of freshly isolated mouse lung cancer LLC- and mouse breast cancer 4T1- derived leptomeningeal metastatic cancer cells from different anatomical locations [RNA-Seq]

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Leptomeningeal metastatic cells outcompete macrophages for iron through Lipocalin-2

Project description:Leptomeningeal metastatic cells outcompete macrophages for iron through Lipocalin-2

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miRNA expression profiles of pediatric medulloblastoma

Project description:The main cause of death in medulloblastoma is recurrence associated with leptomeningeal dissemination. Although the molecular basis of medulloblastoma has received considerable attention over the past decade, the role of microRNAs (miRNAs) in the acquisition of metastatic phenotype remains poorly understood. This study aimed to identify miRNA involved in leptomeningeal dissemination and to elucidate its target mechanisms. We analyzed miRNA expression profiles of 29 medulloblastomas according to the presence of cerebrospinal fluid (CSF) seeding. The differential expressed miRNAs (DEmiRNAs) were validated on 29 medulloblastoma tissues and three medulloblastoma cells. The biological function of the selected miRNA was evaluated using in vitro studies. A total of 12 DEmiRNAs were identified including miRNA-192 in medulloblastoma with seeding. The reduced expression of miRNA-192 was confirmed in tumor seeding group and the medulloblastoma cells. Overexpression of miRNA-192 inhibited cellular proliferation targeting dihydrofolate reductase (DHFR). MiRNA-192 decreased cellular anchoring via repression of integrin subunits (Î±V, Î²1, and Î²3) and CD47. Medulloblastoma with seeding showed specific DEmiRNAs compared with those without seeding. MicroRNA-192 suppresses leptomeningeal dissemination of medulloblastoma through modulating cell proliferation and anchoring ability. leptomeningeal dissemination in 29 pediatric medulloblastoma patients

2015-12-31 | E-GEOD-66968 | biostudies-arrayexpress

Molecular characterization of tumor cells from the cerebrospinal fluid and matched primary tumors from metastatic breast cancer patients with leptomeningeal disease

Project description:We purified tumor cells in the CSF (M-bM-^@M-^\CSFTCM-bM-^@M-^]) from 15 metastatic breast cancer patients diagnosed with leptomeningeal disease using a two-step method involving immunomagnetic enrichment and fluorescence-activated cell sorting (IE/FACS). Magnetic beads coated with mAb to the epithelial cell adhesion marker (EPCAM) were used to enrich for tumor cells and were further purified by FACS analysis. For DNA profiling, isolated CSFTC were subjected to molecular characterization through genome-wide copy number analyses. Genomic analyses were then compared with those performed on the corresponding archival primary tumors. For RNA profiling, isolated CSFTC were then subjected to molecular characterization through gene expression profiling via QPCR analysis of 64 cancer-related genes CGH: 17 CSFTC samples from 13 patients were successfully profiled ,1 patient had 5 timepoints, 6 of 13 patients had matched to copy number data archival tumors RNA: 18 samples from 5 patients had successful gene expression data of the 64 genes measured in triplicates. For non-tumor controls, 9 of the samples had matching gene expression data from sorted leuckocytes (+CD45 cells) obtained from the same draw.

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2024-06-03 | GSE250636 | GEO

Leptomeningeal metastatic cells outcompete macrophages for iron through Lipocalin-2

Project description:The tumor microenvironment plays a critical regulatory role in cancer progression, especially in metastases to the central nervous system. Cancer cells inhabiting the cerebrospinal spinal fluid (CSF)-filled leptomeningeal space face substantial microenvironmental challenges including inflammation and sparse extracellular iron. Unlike CSF leukocytes, we find that cancer cells within the CSF express the iron-binding protein LCN2 and its receptor SCL22A17. Employing mouse models of LM, we find that the LCN2/SLC22A17 system is necessary to support leptomeningeal cancer cell growth. We find that infiltrating CSF macrophages generate inflammatory cytokines that induce cancer cell LCN2 expression. This LCN2/SLC22A17 system provides cancer cells superior access to limiting extracellular iron, allowing LCN2-expressing cancer cells to outcompete CSF macrophages for this resource. Finally, pharmacologic interruption of these interactions prevents cancer cell growth within the leptomeninges.

2020-07-16 | GSE144848 | GEO

Transcriptome of mouse leptomeningeal fibroblats

Project description:Meninges, or the membranous coverings of the brain and spinal cord, play host to dozens of morbid pathologies. In this study we provide a method to isolate the leptomeningeal cell layer, identify leptomeninges in histologic slides, and maintain leptomeningeal fibroblasts in in vitro culture. Using an array of transcriptomic, histological, and cytometric analyses, we identified ICAM1 and SLC38A2 as two novel markers of leptomeningeal cells in vivo and in vitro. Our results confirm the fibroblastoid nature of leptomeningeal cells and their ability to form a sheet-like layer that covers the brain and spine parenchyma. These findings will enable researchers in central nervous system barriers to describe leptomeningeal cell functions in health and disease.

2021-09-29 | GSE150419 | GEO

Molecular characterization of tumor cells from the cerebrospinal fluid and matched primary tumors from metastatic breast cancer patients with leptomeningeal disease

Project description:We purified tumor cells in the CSF (“CSFTC”) from 15 metastatic breast cancer patients diagnosed with leptomeningeal disease using a two-step method involving immunomagnetic enrichment and fluorescence-activated cell sorting (IE/FACS). Magnetic beads coated with mAb to the epithelial cell adhesion marker (EPCAM) were used to enrich for tumor cells and were further purified by FACS analysis. For DNA profiling, isolated CSFTC were subjected to molecular characterization through genome-wide copy number analyses. Genomic analyses were then compared with those performed on the corresponding archival primary tumors. For RNA profiling, isolated CSFTC were then subjected to molecular characterization through gene expression profiling via QPCR analysis of 64 cancer-related genes

2014-01-09 | GSE46068 | GEO

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