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Chitinase-3-like-1 Protein Complexes Modulate Macrophage-Mediated Immune Suppression in Glioblastoma

ABSTRACT: Chitinase-3-like-1 Protein Complexes Modulate Macrophage-Mediated Immune Suppression in Glioblastoma

PROVIDER: PRJNA728678 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14480858_1.fastq.gz	Fastqsanger.gz
	SRR14480858_2.fastq.gz	Fastqsanger.gz
	SRR14480859_1.fastq.gz	Fastqsanger.gz
	SRR14480859_2.fastq.gz	Fastqsanger.gz
	SRR14480860_1.fastq.gz	Fastqsanger.gz

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Chitinase-3-like-1 Protein Complexes Modulate Macrophage-Mediated Immune Suppression in Glioblastoma

Project description:Glioblastoma is a highly malignant and incurable brain tumor characterized by intrinsic and adaptive resistance to immunotherapies. However, how glioma cells induce tumor immunosuppression and escape immunosurveillance remains poorly understood. Here, we find upregulation of cancer-intrinsic Chitinase-3-like-1 (CHI3L1) signaling modulating an immunosuppressive microenvironment by reprogramming tumor-associated macrophages (TAMs). Mechanistically, CHI3L1 binding with Galectin-3 (Gal3) selectively promotes TAM migration and infiltration with a protumor M2-like but not an antitumor M1-like phenotype in vitro and in vivo, governed by a transcriptional program of NFκB/CEBPβ in the CHI3L1/Gal3-PI3K/AKT/mTOR axis. Conversely, Galectin-3-binding protein (Gal3BP) negatively regulates this process by competing with Gal3 to bind CHI3L1. Administration of a Gal3BP mimetic peptide in a syngeneic glioblastoma mouse model reverses immune suppression and attenuates tumor progression. These results shed light on the role of CHI3L1 protein complexes in immune evasion by glioblastoma and as a potential immunotherapeutic target for this devastating disease.

2021-05-11 | GSE174177 | GEO

Chitinase-3-like 1 protein complexes modulate macrophage-mediated immune suppression in glioblastoma.

Project description: Not available

| S-EPMC8363281 | biostudies-literature

Particulate Matter10-induced airway inflammation and fibrosis can be regulated by chitinase-1 suppression

Project description:Particulate matter10 (PM10) can induce airway inflammation and fibrosis. Chitinase-1 is recently known to have key roles in inflammation and fibrosis. We aimed to investigate the effects of chitinase-1 inhibitor in PM10-treated murine models. PM10 and/or OVA-induced airway inflammation and fibrosis murine models were well established. CPX and dexamethasone ameliorated PM10 or PM10/OVA-induced airway hyper-responsiveness, airway inflammation, and fibrosis. CPX and dexamethasone also reduced levels of various inflammatory markers including chitinase-1 in lung homogenates. PM10 and OVA also induced extreme changes of mRNA expression. CPX and dexamethasone decreased levels of mRNA expression especially associated with inflammation and immune regulation. They also significantly regulated asthma and asthma related pathway including JACK-STAT signaling pathway.Chitinase-1 suppression by CPX can regulate PM10-induced and aggravated airway inflammation and fibrosis via various signaling pathway.

2023-01-05 | GSE222111 | GEO

Particulate Matter10-induced airway inflammation and fibrosis can be regulated by chitinase-1 suppression

Project description:Particulate Matter10-induced airway inflammation and fibrosis can be regulated by chitinase-1 suppression

| PRJNA918307 | ENA

Argonaute-miRNA complexes reveal concerted action in disease related pathways of a human, glioblastoma cell line

Project description:Glioblastoma is the most common primary malignant brain tumor occurring in the central nervous system and is characterized by rapid proliferation, genetic aberrations and poor response to treatment. The classical genetic alterations in glioblastoma target pathways governing cellular proliferation, cellular survival, invasion and angiogenesis. In this study, the regulation of glioblastoma-relevant pathways by small non-coding RNAs was analyzed by identification of Argonaute protein-associated microRNAs and mRNAs. We utilized a highly controlled method termed PAR-CLIP-Array by biochemical isolation of cross-linked ribonucleoprotein complexes with monoclonal antibodies specific for individual Argonaute proteins followed by microarray detection. We demonstrate here that the different Argonaute proteins bind different subsets of miRNAs and mRNAs in a glioblastoma cell line model. By extending our study generating miRNA-mRNA network interaction models we could further show, that different Argonaute proteins act in concert to regulate glioblastoma-relevant pathways. We therefore provide novel insights into glioblastoma regulation by microRNAs.

2018-07-18 | GSE30730 | GEO

BCL7A-containing SWI/SNF/BAF complexes modulate mitochondrial bioenergetics during neural progenitor differentiation.

Project description:BCL7A-containing SWI/SNF/BAF complexes modulate mitochondrial bioenergetics during neural progenitor differentiation.

| PRJNA867373 | ENA

BCL7A-containing SWI/SNF/BAF complexes modulate mitochondrial bioenergetics during neural progenitor differentiation.

Project description:BCL7A-containing SWI/SNF/BAF complexes modulate mitochondrial bioenergetics during neural progenitor differentiation.

| PRJNA867370 | ENA

BCL7A-containing SWI/SNF/BAF complexes modulate mitochondrial bioenergetics during neural progenitor differentiation.

Project description:BCL7A-containing SWI/SNF/BAF complexes modulate mitochondrial bioenergetics during neural progenitor differentiation.

| PRJNA867374 | ENA

BCL7A-containing SWI/SNF/BAF complexes modulate mitochondrial bioenergetics during neural progenitor differentiation.

Project description:BCL7A-containing SWI/SNF/BAF complexes modulate mitochondrial bioenergetics during neural progenitor differentiation.

| PRJNA867378 | ENA

Distinct roles of HDAC complexes in promoter silencing, antisense suppression and DNA damage protection

Project description:Histone acetylation plays an important role in regulating DNA accessibility. Multifunctional Sin3 proteins bind histone deacetylases (HDACs) to assemble silencing complexes that selectively target chromatin. We show that, in fission yeast, an essential HDAC Clr6 exists in two distinct Sin3 core complexes. Complex I contains an essential Sin3 homologue Pst1 and other factors, and predominantly targets gene promoters. Complex II contains a non-essential Sin3, Pst2, and several conserved proteins. It preferentially targets transcribed chromosomal regions and centromere cores. Defects in complex II abrogate global protective functions of chromatin, causing increased accessibility of DNA to genotoxic agents and widespread antisense transcripts that are processed by the exosome. Interestingly, the two Clr6 complexes differentially repress forward and reverse centromeric repeat transcripts, suggesting that these complexes regulate transcription in heterochromatin and euchromatin in a similar manner, including suppression of spurious transcripts from cryptic start sites. This SuperSeries is composed of the SubSeries listed below.

2007-04-23 | GSE7160 | GEO

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