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Glioma-initiating cells at tumor edge gain signals from tumor core cells to promote their malignancy

ABSTRACT: Glioma-initiating cells at tumor edge gain signals from tumor core cells to promote their malignancy

PROVIDER: PRJNA643851 | ENA |

REPOSITORIES: ENA

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Glioma-initiating cells at tumor edge gain signals from tumor core cells to promote their malignancy

Project description:Intratumor spatial heterogeneity facilitates therapeutic resistance in glioblastoma (GBM). Nonetheless, understanding of GBM is limited to the resectable tumor core lesion while the seeds for recurrence reside in the unresectable tumor edge. In this study, stratification of GBM to core and edge demonstrated clinically relevant surgical sequelae. We establish regionally derived models of GBM edge and core that retain their spatial identity in a cell autonomous manner. Edge cells show a higher capacity for infiltrative growth, while core cells demonstrate greater therapy resistance. Investigation of intercellular signaling between these two cell populations uncovered the paracrine crosstalk from tumor core that provokes malignancy and therapy resistance of edge cells. These phenotypic alterations were initiated by HDAC1 in GBM core cells which subsequently affect edge cells by secreting the soluble form of CD109 protein. Our data reveal the role of intracellular communication between regionally different populations of GBM cells in tumor recurrence.

2020-07-03 | GSE153746 | GEO

Glioma-initiating cells at tumor edge gain signals from tumor core cells to promote their malignancy.

Project description: Not available

| S-EPMC7494913 | biostudies-literature

Crosstalk with astrocytes establishes tumor edge in glioblastoma

Project description:Clinical outcomes for patients with glioblastoma (GBM) are extremely poor due to inevitable tumor recurrence even after extensive treatments. These recurrences are thought to manifest from cells located within the tumor edge. Despite this, the precise molecular mechanism governing GBM spatial phenotypic heterogeneity (e.g. edge vs. core) and subsequent tumor recurrence remains poorly elucidated. Here, using patient-derived GBM core and edge tissues, we analyzed transcriptional and metabolic signatures in an effort to determine how GBM facilitates the edge phenotype and its associated recurrence-initiating cells (RICs). In so doing, we unexpectedly identified CD38 as an essential protein in the formation of the edge phenotype and found a CD38-driven interaction between edge GBM cells and neighboring astrocytes that communally develops a GBM edge that is unresectable by surgery and retains RICs.

2021-12-25 | GSE135408 | GEO

Crosstalk with astrocytes establishes tumor edge in glioblastoma

Project description:Crosstalk with astrocytes establishes tumor edge in glioblastoma

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Mouse mammary tumor-initiating cells

Project description:Using a syngeneic p53 null mouse mammary gland tumor model that closely mimics human breast cancer, we have identified by limiting dilution transplantation as well as in vitro mammosphere and clonogenic assays a Lin-CD29HighCD24High subpopulation of tumor-initiating cells. Differentially expressed genes in the Lin-CD29HighCD24High mouse mammary gland tumor-initiating cell population include those involved in DNA damage response and repair, as well as genes involved in epigenetic regulation previously shown to be critical for stem cell self-renewal. Keywords: tumor-initiating cells

2008-06-27 | GSE8863 | GEO

Multi-omics analysis of spatially distinct stromal cells reveals tumor-induced O-glycosylation of the CDK4-pRB axis in fibroblasts at the invasive tumor edge

Project description:The invasive leading edge represents a potential gateway for tumor metastasis. The role of fibroblasts from the tumor edge in promoting cancer invasion and metastasis has not been comprehensively elucidated. We hypothesize that crosstalk between tumor and stromal cells within the tumor microenvironment (TME) results in activation of key biological pathways depending on their position in the tumor (edge vs core). Here we highlight phenotypic differences between tumor-adjacent-fibroblasts (TAF) from the invasive edge and tumor core fibroblasts (TCF) from the tumor core, established from human lung adenocarcinomas. A multi-omics approach that includes genomics, proteomics, and O-glycoproteomics was used to characterize crosstalk between TAFs and cancer cells. These analyses showed that O-glycosylation, an essential post-translational modification resulting from sugar metabolism, alters key biological pathways including the cyclin-dependent kinase 4 and phosphorylated retinoblastoma protein (CDK4-pRB) axis in the stroma and indirectly modulates pro-invasive features of cancer cells. In summary, the O-glycoproteome represents a new consideration for important biological processes involved in tumor-stroma crosstalk and a potential avenue to improve the anti-cancer efficacy of CDK4 inhibitors.

2021-10-22 | GSE186235 | GEO

Myeloid amino acid metabolism supports solid tumor malignancy

Project description:Myeloid amino acid metabolism supports solid tumor malignancy

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Expression data from mouse liver tumor-initiating cells

Project description:The Toll-like receptor 4 (TLR4) pathway is important for tumor-initiating cells. We used microarrays to obtain gene profiling data in order to increase understanding of the pathways. Liver tumor-initiating cells were used for RNA extraction and hybridization on Affymetrix microarrays.

2013-03-30 | E-GEOD-45646 | biostudies-arrayexpress

Brain tumor initiating cell response to microglia

Project description:Determination of the mechanism by which microglia regulate growth of brain tumor initiating cells (BTICs) and differentiation. Results identify the factors involved in the regulation and provide mechanistic basis. We subjected brain tumor initiating cells to microarray to determine the genes involved in BTICs growth and differentiation when exposed to microglia conditioned medium (MCM) for 6h.

2013-11-06 | GSE52127 | GEO

Immune Resistance Emerges from Tumor-Initiating Stem Cells

Project description:Immune Resistance Emerges from Tumor-Initiating Stem Cells

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