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

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

PROVIDER: PRJNA634910 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11843759.fastq.gz	Fastqsanger.gz
	SRR11843760.fastq.gz	Fastqsanger.gz
	SRR11843761.fastq.gz	Fastqsanger.gz
	SRR11843762.fastq.gz	Fastqsanger.gz
	SRR11843763.fastq.gz	Fastqsanger.gz

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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

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

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

2015-06-29 | GSE68800 | GEO

Musashi1 Contribution 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 levels are often observed in tumors with numerous oncogenic RBPs identified in recent years. Musashi1 (Msi1) is an RBP and stem cell gene that controls the balance between self-renewal and differentiation. High Msi1 levels have been observed in multiple tumors including glioblastoma and are often associated with poor patient outcomes and tumor growth. A comprehensive genomic analysis identified a network of cell cycle/division and DNA replication genes and established these processes as Msi1's core regulatory functions in glioblastoma. Msi1 controls this gene network via two mechanisms: direct interaction and indirect regulation mediated by the transcription factors E2F2 and E2F8. Moreover, glioblastoma lines with Msi1 knockout (KO) displayed increased sensitivity to cell cycle and DNA replication inhibitors. Our results suggest that a drug combination strategy (Msi1 + cell cycle/DNA replication inhibitors) could be a viable route to treat glioblastoma.

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BCAT1 regulates glioblastoma cell plasticity and contributes to immunosuppression

Project description:BCAT1 regulates glioblastoma cell plasticity and contributes to immunosuppression

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GDNF/GFRA1 signaling contributes to chemo- and radioresistance in glioblastoma

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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.

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

Project description:Musashi1 targeted expression in murine intestine

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Genomic-Enabled Medicine for Recurrent Glioblastoma

Project description:<p>In this prospective study, we performed genome-wide tumor/normal exome sequencing and tumor RNA-sequencing for recurrent glioblastoma patients. A subset of patients had both enhancing tumor and non-enhancing tissue sequenced to investigate spatial heterogeneity of this disease. Together, this information builds our understanding of the genomic underpinnings of glioblastoma, and contributes toward the knowledge base for identifying and developing more effective treatments for patients with glioblastoma.</p>

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BCAT1 regulates glioblastoma cell plasticity and contributes to immunosuppression

Project description:Glioblastoma is the most common malignant brain tumor in adults. Cellular plasticity and the poorly differentiated features result in a fast relapse of the tumors following treatment. Moreover, the immunosuppressive microenvironment proved to be a major obstacle to immunotherapeutic approaches. Branched-chain amino acid transaminase 1 (BCAT1) is a metabolic enzyme that converts branched-chain amino acids into branched-chain keto acids, depleting cellular α-ketoglutarate and producing glutamate. BCAT1 was shown to drive the growth of glioblastoma and other cancers; however, its oncogenic mechanism remains poorly understood. Here, we show that BCAT1 is crucial for maintaining the poorly differentiated state of glioblastoma cells and that its low expression correlates with a more differentiated glioblastoma phenotype. Furthermore, orthotopic tumor injection into immunocompetent mice demonstrated that the brain microenvironment is sufficient to induce differentiation of Bcat1-KO tumors in vivo. We link the transition to a differentiated cell state to the increased activity of TET demethylases and the hypomethylation and activation of neuronal differentiation genes. In addition, the knockout of Bcat1 attenuated immunosuppression, allowing for an extensive infiltration of CD8 + cytotoxic T-cells and complete abrogation of tumor growth. Further analysis in immunodeficient mice revealed that both tumor cell differentiation and immunomodulation following BCAT1-KO contribute to the long-term suppression of tumor growth. In summary, our study unveils BCAT1's pivotal role in promoting glioblastoma growth by inhibiting tumor cell differentiation and sustaining an immunosuppressive milieu. These findings offer a novel therapeutic avenue for targeting glioblastoma through the inhibition of BCAT1.

2024-11-08 | GSE247299 | GEO

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