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MSI1 promotes the expression of the GBM stem cell marker CD44 by impairing miRNA-dependent degradation. [miRNA-Seq]

ABSTRACT: MSI1 promotes the expression of the GBM stem cell marker CD44 by impairing miRNA-dependent degradation. [miRNA-Seq]

PROVIDER: PRJNA670370 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12856990.fastq.gz	Fastqsanger.gz
	SRR12856991.fastq.gz	Fastqsanger.gz
	SRR12856992.fastq.gz	Fastqsanger.gz
	SRR12856993.fastq.gz	Fastqsanger.gz
	SRR12856994.fastq.gz	Fastqsanger.gz

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MSI1 promotes the expression of the GBM stem cell marker CD44 by impairing miRNA-dependent degradation.

Project description:MSI1 promotes the expression of the GBM stem cell marker CD44 by impairing miRNA-dependent degradation.

| PRJNA670361 | ENA

MSI1 promotes the expression of the GBM stem cell marker CD44 by impairing miRNA-dependent degradation. [miRNA-Seq]

Project description:The stem cell marker Musashi1 (MSI1) is highly expressed during neurogenesis and in Glioblastoma (GBM). In cancer and non-malignant progenitor cells, MSI1 promotes self-renewal and impairs differentiation, involving the regulation of mRNA translation. However, a comprehensive understanding of MSI1’s role in promoting GBM-driving networks remains to be deciphered.

2020-12-15 | GSE159738 | GEO

MSI1 promotes the expression of the GBM stem cell marker CD44 by impairing miRNA-dependent degradation. [RNA-Seq]

2020-12-15 | GSE159739 | GEO

MSI1 promotes the expression of the GBM stem cell marker CD44 by impairing miRNA-dependent degradation. [RNA-Seq II]

2020-12-15 | GSE159889 | GEO

MSI1 promotes the expression of the GBM stem cell marker CD44 by impairing miRNA-dependent degradation. [RNA-Seq]

Project description:MSI1 promotes the expression of the GBM stem cell marker CD44 by impairing miRNA-dependent degradation. [RNA-Seq]

| PRJNA670371 | ENA

MSI1 promotes the expression of the GBM stem cell marker CD44 by impairing miRNA-dependent degradation. [RNA-Seq II]

Project description:MSI1 promotes the expression of the GBM stem cell marker CD44 by impairing miRNA-dependent degradation. [RNA-Seq II]

| PRJNA670729 | ENA

MSI1 Promotes the Expression of the GBM Stem Cell Marker CD44 by Impairing miRNA-Dependent Degradation.

Project description:The stem cell marker Musashi1 (MSI1) is highly expressed during neurogenesis and in glioblastoma (GBM). MSI1 promotes self-renewal and impairs differentiation in cancer and non-malignant progenitor cells. However, a comprehensive understanding of its role in promoting GBM-driving networks remains to be deciphered. We demonstrate that MSI1 is highly expressed in GBM recurrences, an oncologist's major defiance. For the first time, we provide evidence that MSI1 promotes the expression of stem cell markers like CD44, co-expressed with MSI1 within recurrence-promoting cells at the migrating front of primary GBM samples. With GBM cell models of pediatric and adult origin, including isolated primary tumorspheres, we show that MSI1 promotes stem cell-like characteristics. Importantly, it impairs CD44 downregulation in a 3'UTR- and miRNA-dependent manner by controlling mRNA turnover. This regulation is disturbed by the previously reported MSI1 inhibitor luteolin, providing further evidence for a therapeutic target potential of MSI1 in GBM treatment.

| S-EPMC7762192 | biostudies-literature

MSI1 promotes the expression of the GBM stem cell marker CD44 by impairing miRNA-dependent degradation.

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

2020-12-15 | GSE159740 | GEO

miRNA profiles in Primary and Recurrent GBM

Project description:Glioblastoma (GBM) bears a dismal prognosis with rapid relapse following complete resection and radiochemotherapy. The involvement of microRNAs in tumor progression has been demonstrated in hepatoma, breast cancer, and prostate cancers. However, the microRNAs involved in modulating the progression and relapse of GBM are still unclear. Initially, we compared the miRNA expression profiles between primary and recurrent GBM tissues from the same patient in twelve independent cases. miRNA expression profiles between primary and recurrent GBM tissues from the same patient in twelve independent cases.

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Abemaciclib reduces glioblastoma stemness by targeting the GSK3b-mediated transcriptional regulation of CD44 and TCF7L2.

Project description:Glioblastoma multiforme (GBM) is the most common and deadliest glioma, originating from astrocytic progenitors or stem cells and affecting individuals of all ages. Current treatments include surgery, radiation therapy, chemotherapy, and combinations of these modalities. Temozolomide, the first-line chemotherapy for GBM, improves survival when combined with radiation but has limited success due to the tumor's inherent resistance to therapies. Cancer stem cells (CSCs), which exhibit self-renewal and differentiation capabilities, contribute to therapeutic resistance, making them a promising target for GBM therapy. Abemaciclib, a CDK4/6 inhibitor, effectively reduces tumor growth and sphere formation in GBM, although its exact mechanism remains unclear. Our data revealed that Abemaciclib significantly inhibited tumor sphere formation in U87MG and KNS42 cells by downregulating epithelial-mesenchymal transition (EMT)-associated genes, including CD44 and TCF7L2. Notably, silencing CD44 and TCF7L2 also led to a marked reduction in sphere formation. Phospho-kinase array analysis revealed that Abemaciclib reduces pGSK3β and pCREB in sphere cells. Western blotting confirmed that Abemaciclib diminishes pGSK3β-Y216 in parental cells, suggesting reduced kinase activity. Pharmacological inhibition of GSK3β also decreased CD44 and TCF7L2 expression. In an orthotopic animal model, Abemaciclib inhibited tumor formation, with reduced levels of pRB, pGSK3β, Ki67, and CD44 confirmed by immunohistochemistry. Analysis of TCGA and CGGA datasets showed that the mesenchymal GBM subtype (MES-GBM), associated with poor prognosis, has higher EMT gene expression. Treatment of MES-like LN229 cells with Abemaciclib decreased EMT-related genes. These findings suggest that Abemaciclib disrupts GSK3β-mediated EMT pathways, impairing CSC self-renewal and offering a potential therapeutic strategy for GBM.

2025-03-12 | GSE290174 | GEO

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