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A mouse model of targeted Musashi1 expression in whole intestinal epithelium unveils its major roles in cell cycle and stemness

ABSTRACT: Musashi1 targeted expression in murine intestine

PROVIDER: PRJEB7280 | ENA |

REPOSITORIES: ENA

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A Mouse Model of Targeted Musashi1 Expression in Whole Intestinal Epithelium Suggests Regulatory Roles in Cell Cycle and Stemness.

Project description:The intestinal epithelium is very peculiar for its continuous cell renewal, fuelled by multipotent stem cells localized within the crypts of Lieberkühn. Several lines of evidence have established the evolutionary conserved RNA-binding protein Musashi1 as a marker of adult stem cells, including those of the intestinal epithelium, and revealed its roles in stem cell self-renewal and cell fate determination. Previous studies from our laboratories have shown that Musashi1 controls stem cell-like features in medulloblastoma, glioblastoma, and breast cancer cells, and has pro-proliferative and pro-tumorigenic properties in intestinal epithelial progenitor cells in vitro. To undertake a detailed study of Musashi1's function in the intestinal epithelium in vivo, we have generated a mouse model, referred to as v-Msi, overexpressing Musashi1 specifically in the entire intestinal epithelium. Compared with wild type litters, v-Msi1 mice exhibited increased intestinal crypt size accompanied by enhanced proliferation. Comparative transcriptomics by RNA-seq revealed Musashi1's association with gut stem cell signature, cell cycle, DNA replication, and drug metabolism. Finally, we identified and validated three novel mRNA targets that are stabilized by Musashi1, Ccnd1 (Cyclin D1), Cdk6, and Sox4. In conclusion, the targeted expression of Musashi1 in the intestinal epithelium in vivo increases the cell proliferation rate and strongly suggests its action on stem cells activity. This is due to the modulation of a complex network of gene functions and pathways including drug metabolism, cell cycle, and DNA synthesis and repair.

| S-EPMC4713339 | biostudies-literature

The RNA-binding protein Musashi1 is a central regulator of adhesion pathways in glioblastoma

Project description:The conserved RNA-binding protein Musashi1 (MSI1) has emerged as a key oncogenic factor in numerous solid tumors, including glioblastoma. However, its mechanism of action has not yet been established comprehensively. We set out to map its impact on the transcriptome in U251 cells using RNA-seq and iCLIP. Examination of gene expression and splicing changes upon KD of Musashi1 in U251 cells and link to iCLIP-identified Musashi1 RNA binding sites

2015-06-29 | E-GEOD-68800 | biostudies-arrayexpress

Different gene expression of Musashi1 gene overexpression in mouse skin

Project description:To further understand expression patterns of musashi1 overexpression (DTG) in mouse skin,we have employed microarray expression profiling as a discovery platform to identify different genes expression with DTG mouse and Control mouse. Comparision with Control mouse,upgene is 3772 in DTG mouse, downgene is 5529. mTOR pathway, RAS pathway, PI3K-AKT pathway,IL6-JAK-Stat3 pathway and so on are activated, WNT Pathway is inhibited.

2020-11-12 | GSE117284 | GEO

The RNA-binding protein Musashi1 is a central regulator of adhesion pathways in glioblastoma

2015-06-29 | GSE68800 | GEO

Musashi1 contributes to glioblastoma development via regulation of a network of DNA replication, cell cycle, and division genes

Project description:RNA binding proteins (RBPs) function as master regulators of gene expression. Alterations in their expression levels and function are often observed in tumors with numerous oncogenic RBPs identified in recent years. Musashi1 (Msi1) is an RBP and stem cell marker gene that controls the balance between self-renewal and proliferation. High Msi1 levels have been observed in multiple tumor types including glioblastoma and are often associated with poor patient outcomes. Msi1 knockdown is known to affect numerous cancer phenotypes and to prevent growth of different tumor types. To dissect Msi1’s main contributions to glioblastoma development, we conducted a comprehensive genomic analysis. We identified a network of cell cycle/division and DNA replication genes and established these processes as its core functions. Msi1 controls this gene network via two mechanisms: direct interaction and indirect regulation mediated by the transcription factors E2F2 and E2F8. We corroborated Msi1’s impact on these processes and determined that glioblastoma lines with Msi1 KO display increased sensitivity to cell cycle and DNA replication inhibitors. As Msi1 inhibitors have been identified, a drug combination strategy (Msi1 + cell cycle/DNA replication inhibitors) could be a viable route to treat glioblastoma.

2020-07-08 | GSE151155 | GEO

Different gene expression of Musashi1 gene overexpression in mouse skin

Project description:Different gene expression of Musashi1 gene overexpression in mouse skin

| PRJNA481661 | ENA

Musashi1 is a master regulator of aberrant translation in Group 3 medulloblastoma

Project description:Musashi1 is a master regulator of aberrant translation in Group 3 medulloblastoma

| PRJNA555800 | ENA

Musashi1 contributes to glioblastoma development via regulation of a network of DNA replication, cell cycle, and division genes

Project description:Musashi1 contributes to glioblastoma development via regulation of a network of DNA replication, cell cycle, and division genes

| PRJNA634910 | ENA

Image based identification and targeting of cancer stem cells in pancreatic adenocarcinoma (PDAC)

2016-06-15 | GSE75797 | GEO

Image based identification and targeting of cancer stem cells in pancreatic adenocarcinoma (PDAC)

Project description:Purpose: The goals of this study were to identify quantitative gene expression differences between wild type, Musashi1 null, Msuashi2 null and Musashi1/Musashi2 null MIAPaCa2 pancreatic cancer cells mRNA profiles of MIA PaCa-2 cancer cells were generated by deep sequencing, in triplicate, using Illumina HiSeq2500.

2016-06-15 | E-GEOD-75797 | biostudies-arrayexpress

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