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

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE159740 | 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.

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. [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.

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]

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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]

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CD44 promotes Kras-dependent lung adenocarcinoma.

Project description:Kras-induced non-small-cell lung adenocarcinoma is the major subtype of lung cancers and is associated with poor prognosis. Using a lung cancer mouse model that expresses a cre-mediated KrasG12D mutant, we identified a critical role for the cell surface molecule CD44 in mediating cell proliferation downstream of oncogenic Kras signaling. The deletion of CD44 attenuates lung adenocarcinoma formation and prolongs the survival of these mice. Mechanistically, CD44 is required for the activation of Kras-mediated signaling through the mitogen-activated protein kinase (MAPK) pathway and thus promotes tumor cell proliferation. Together, these results reveal an unrecognized role for CD44 in oncogenic Kras-induced lung adenocarcinoma and suggest that targeting CD44 could be an effective strategy for halting Kras-dependent carcinomas.

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PDRG1 promotes the proliferation and migration of GBM cells by the MEK/ERK/CD44 pathway.

Project description:P53 and DNA damage-regulated gene1 (PDRG1) is overexpressed in diverse carcinomas. Here, we discover that PDRG1 is overexpressed in glioblastoma multiforme (GBM). However, the clinical significance, biological role, and underlying molecular mechanisms of PDRG1 in GBM remain unclear. PDRG1 was aberrantly overexpressed in glioma, especially prevalent in GBM, and correlated with poor clinicopathologic features of glioma. The risk score, operational feature curve analysis, Kaplan-Meier curve, and univariate and multivariate Cox regression analysis indicated that PDRG1 was an independent prognostic indicator and significantly correlates with disease progression of glioma. A prognostic nomogram was constructed to predict the survival risk of individual patients. The function and pathway enrichment analysis of PDRG1 in The Cancer Genome Atlas cohort was performed. PDRG1 knockdown significantly inhibited the migration and proliferation of GBM cells in vitro and in vivo. Transcriptome sequencing analysis of PDRG1 knockdown U-118 MG(U118) cells indicated that biological regulation adhesion, growth and death, cell motility, cell adhesion molecular and proteoglycans in cancer were significantly enriched. Importantly, we found that the expression of adhesion molecule cluster of differentiation 44 (CD44) was regulated by PDRG1 in GBM. We found that PDRG1 promoted the migration and proliferation of GBM cells via the mitogen-activated protein kinase kinase (MEK)/extracellular regulated protein kinase (ERK)/CD44 pathway. Our findings provide proof that PDRG1 upregulation predicts progression and poor prognosis in human gliomas, especially in isocitrate dehydrogenase (IDH) wt glioma patients. The study provides new evidence that PDRG1 regulates the expression of CD44 in GBM cells and might promote the migration and proliferation via the MEK/ERK/CD44pathway. PDRG1 might be a novel diagnostic indicator and promising therapeutic target for GBM.

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