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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE159738 | GEO | 2020/12/15

REPOSITORIES: GEO

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

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

| PRJNA670370 | ENA

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:This SuperSeries is composed of the SubSeries listed below.

2020-12-15 | GSE159740 | GEO

Msi1 assists CPEB1-driven polyadenylation [Msi1 RIP]

Project description:The translational reactivation of maternal mRNAs encoding the drivers of vertebrate meiosis is accomplished mainly by cytoplasmic polyadenylation. The Cytoplasmic Polyadenylation Elements (CPEs) present in the 3’ UTR of these transcripts, together with their cognate CPE-binding proteins (CPEBs), define a combinatorial code that determines the timing and extent of translational activation upon meiosis resumption. In addition, the RNA-binding protein Musashi1 (Msi1) regulates the polyadenylation of CPE-containing mRNAs by an as yet undefined CPEB-dependent or -independent mechanism. Here we show that Msi1 alone does not support cytoplasmic polyadenylation, but its binding triggers the remodeling of RNA structure, thereby exposing adjacent CPEs and stimulating polyadenylation. Thus, Msi1 directs the preferential use of specific CPEs, which in turn affects the timing and extent of polyadenylation during meiotic progression. Genome-wide analysis of CPEB1- and Msi-associated mRNAs identified 491 common targets, thus revealing a new layer of CPE-mediated translational control.

2017-07-17 | GSE68097 | GEO

Msi1 assists CPEB1-driven polyadenylation [CPEB1 & Msi1 RIP replicate]

2017-07-17 | GSE68095 | GEO