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Chi3l1 is a modulator of glioma stem cell states and a therapeutic vulnerability for glioblastoma [RNA-seq]

ABSTRACT: Chi3l1 is a modulator of glioma stem cell states and a therapeutic vulnerability for glioblastoma [RNA-seq]

PROVIDER: PRJNA765690 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16027494_1.fastq.gz	Fastqsanger.gz
	SRR16027494_2.fastq.gz	Fastqsanger.gz
	SRR16027495_1.fastq.gz	Fastqsanger.gz
	SRR16027495_2.fastq.gz	Fastqsanger.gz
	SRR16027496_1.fastq.gz	Fastqsanger.gz

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Chi3l1 is a modulator of glioma stem cell states and a therapeutic vulnerability for glioblastoma [scRNA-seq]

Project description:Chi3l1 (Chitinase 3-like 1) is a secreted protein highly expressed in glioblastoma. Here, we show that exposure of glioma stem cells (GSCs) to Chi3l1 reduces the CD133+/SOX2+ cells and increases the CD44+/Chi3l1+ cells. Single cell RNA-seq and RNA velocity following incubation of GSCs with Chi3l1 show significant changes in GSC state dynamics driving GSCs towards a mesenchymal expression profile and reducing transition probabilities towards terminal cellular states. ATAC-seq reveals that Chi3l1 increases accessibility of promoters containing MAZ transcription factor footprint. Inhibition of MAZ directly regulates genes with highest expression in cellular clusters exhibiting significant cell state transitions.

2022-10-24 | GSE184696 | GEO

Chi3l1 is a modulator of glioma stem cell states and a therapeutic vulnerability for glioblastoma [RNA-seq]

2022-10-24 | GSE184695 | GEO

Chi3l1 is a modulator of glioma stem cell states and a therapeutic vulnerability for glioblastoma

Project description:Chi3l1 is a modulator of glioma stem cell states and a therapeutic vulnerability for glioblastoma

| PRJNA765679 | ENA

Chi3l1 is a modulator of glioma stem cell states and a therapeutic vulnerability for glioblastoma [scRNA-seq]

Project description:Chi3l1 is a modulator of glioma stem cell states and a therapeutic vulnerability for glioblastoma [scRNA-seq]

| PRJNA765691 | ENA

Antibody blockade resets CHI3L1-induced glioma stem cell phenotypic transitions and reduces glioblastoma tumor burden

Project description:CHI3L1 (Chitinase 3-like1) is one of the highest expressed genes in glioblastoma and is associated with therapy resistance and low survival of patients. Here, we show that exposure of glioma stem cells (GSCs) to CHI3L1 induces marked phenotypic and transcriptomic change from CD133+/SOX2+ pro-neural to CD44+/CHI3L1+ mesenchymal phenotype. CHI3L1 induces chromatin remodeling in GSCs and regulates accessibility of ZNF281, CTCFL, SOX9, and the OCT4-SOX2-TCF3-NANOG transcription factor complex that drive the CHI3L1-mediated mesenchymal “switch” and maintain GSC identity.

2022-10-24 | GSE154060 | GEO

Chi3l1 is a modulator of glioma stem cell states and a therapeutic vulnerability for glioblastoma

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-10-24 | GSE184698 | GEO

Chi3l1 Is a Modulator of Glioma Stem Cell States and a Therapeutic Target in Glioblastoma.

Project description:Chitinase 3-like 1 (Chi3l1) is a secreted protein that is highly expressed in glioblastoma. Here, we show that Chi3l1 alters the state of glioma stem cells (GSC) to support tumor growth. Exposure of patient-derived GSCs to Chi3l1 reduced the frequency of CD133+SOX2+ cells and increased the CD44+Chi3l1+ cells. Chi3l1 bound to CD44 and induced phosphorylation and nuclear translocation of β-catenin, Akt, and STAT3. Single-cell RNA sequencing and RNA velocity following incubation of GSCs with Chi3l1 showed significant changes in GSC state dynamics driving GSCs towards a mesenchymal expression profile and reducing transition probabilities towards terminal cellular states. ATAC-seq revealed that Chi3l1 increases accessibility of promoters containing a Myc-associated zinc finger protein (MAZ) transcription factor footprint. Inhibition of MAZ downregulated a set of genes with high expression in cellular clusters that exhibit significant cell state transitions after treatment with Chi3l1, and MAZ deficiency rescued the Chi3L-induced increase of GSC self-renewal. Finally, targeting Chi3l1 in vivo with a blocking antibody inhibited tumor growth and increased the probability of survival. Overall, this work suggests that Chi3l1 interacts with CD44 on the surface of GSCs to induce Akt/β-catenin signaling and MAZ transcriptional activity, which in turn upregulates CD44 expression in a pro-mesenchymal feed-forward loop. The role of Chi3l1 in regulating cellular plasticity confers a targetable vulnerability to glioblastoma.SignificanceChi3l1 is a modulator of glioma stem cell states that can be targeted to promote differentiation and suppress growth of glioblastoma.

| S-EPMC10267676 | biostudies-literature

A clinically applicable connectivity signature for glioblastoma includes the tumor network driver CHI3L1

Project description:Tumor microtubes (TMs) connect glioma cells to a network with considerable relevance for tumor progression and therapy resistance. The determination of TM-interconnectivity in individual tumors has been challenging and the impact on patient survival unresolved. Here, a connectivity signature from single-cell RNA-sequenced (scRNA-Seq) xenografted primary glioblastoma (GB) cells has been established using a dye uptake methodology, confirmed with recording of cellular calcium epochs and validated with clinical correlations. Astrocyte-like and mesenchymal-like GB cells have the highest connectivity signature scores in scRNA-sequenced patient-derived xenografts and patient samples. In large GB cohorts, network connectivity correlated with the mesenchymal subtype and dismal patient survival. CHI3L1 has been identified and validated as a robust molecular marker of connectivity with functional relevance. The connectivity signature allows novel insights into brain tumor biology, provides a proof-of-principle that tumor cell TM-connectivity is relevant for patients’ prognosis, and serves as a robust prognostic biomarker.

2023-11-27 | PXD044001 | Pride

CHI3L1 regulates papillary thyroid tumor progression via TP53 signaling

Project description:Purpose: This study aimed to investigate the potential impacts of the CHI3L1 gene on the progression of papillary thyroid carcinoma (PTC) and to propose novel therapeutic approaches. Methods: CHI3L1 expression in PTC was analyzed using public datasets. Cell proliferation was assessed using the CCK-8 assay and colony formation assay. Tumor growth was evaluated using nude mouse xenograft models. Cell invasion was evaluated using the transwell assay, while cell migration was assessed with the wound healing assay. Transcriptomic analysis was conducted to examine the molecular mechanism, and real-time quantitative PCR was performed for gene expression validation. Results: The findings revealed that CHI3L1 expression was upregulated in various cancers, mainly in PTC. Both in vitro and in vivo assays demonstrated that cell proliferation was suppressed when CHI3L1 was knocked down. Transcriptome sequencing indicated that CHI3L1 knockdown was associated with migration-related pathways and TP53 signaling pathway. Transwell assays showed reduced cell invasion upon CHI3L1 suppression, while wound healing assays demonstrated decreased cell migration. Following CHI3L1 silencing, real-time quantitative PCR verified the overexpression of TP53-related genes. Survival analysis further indicated a correlation between elevated CHI3L1 expression and reduced survival rates. Conclusion: This study identified that CHI3L1 was an oncogene in human papillary thyroid cells and suggested that it may influence tumorigenesis through the TP53 signaling pathway. Thus, CHI3L1 could serve as a potential therapeutic target for PTC patients.

2025-01-02 | GSE285569 | GEO

Transcriptome analysis of Chi3l1-deficient TFH cells

Project description:To better understand how Chi3l1 regulates the TFH response, we analyzed the transcriptome of CXCR5+PD1+CD4+Lin- TFH cells from msLNs of WT and Chi3l1-/- mice on D14 post H. pylori infection.

2023-07-19 | GSE203113 | GEO

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