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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]

| 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

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.

| S-EPMC4227610 | biostudies-literature

Whether CD44 is an applicable marker for glioma stem cells.

Project description:Glioblastoma multiforme (GBM) is one of the most malignant and aggressive brain tumors with great amount of hyaluronan (HA) secretion and CD44 overexpression (HA receptor). CD44 has been suggested as a cancer stem cells (CSCs) marker. However, several clinical studies have indicated that CD44low glioma cell exhibit CSCs traits. Additionally, our previous study indicated that more CD44 expression was associated with a better prognosis in GBM patients. To determine whether CD44 is an appropriate marker of glioma stem cells (GSCs), we manipulated CD44 expression using intrinsic (CD44 knockdown, CD44kd) and extrinsic (HA supplement, HA+) methods. Our results show that CD44kd suppressed cell proliferation by retarding cell cycle progression from G0/G1 to S phase. Furthermore, it caused GSCs traits, including lower expression of differentiation marker (glial fibrillary acidic protein, GFAP), a higher level of sphere formation and higher expression of stem cell markers (CD133, nestin and Oct4). The reduction of CD44 expression induced by HA+ was accompanied by an increase in GSCs properties. Interestingly, the presence of HA+ in glioma cells with GSC traits conversely facilitated differentiation. Our data indicated that the CD44 low-expressing cells exhibit more GSCs straits, suggesting that CD44 is not an appropriate marker for GSCs. Furthermore, the preferential expression of CD44 at the invasive rim in rat glioma specimen implies that CD44 may be more important for invasion and migration instead of GSCs marker in glioma.

| S-EPMC5714766 | biostudies-literature

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