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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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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.

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

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

Project description:Glioblastoma (GBM) is the most common primary brain tumor in adults, characterized by an inherent aggressivity and resistance to treatment leading to poor prognoses. While some resistance mechanisms have been elucidated, a deeper understanding of these mechanisms is needed to increase therapeutic efficacy. In this study we first discovered glial-cell derived neurotrophic factor (GDNF) to be upregulated in patient-derived glioblastoma spheroid cultures after chemotherapeutic temozolomide (TMZ) treatment, through RNA-Seq experiments. Therefore, we investigated the role of the GDNF/GDNF receptor alpha 1 (GFRA1) signaling pathway as a resistance mechanism to chemotherapy with temozolomide and lomustine as well as irradiation using patient-derived glioblastoma spheroid cultures. With qPCR experiments we showed a consistent upregulation of GDNF and its primary receptor GFRA1 following all three lines of treatment. Moreover, CRISPR/Cas9 knock-outs of GDNF in two patient-derived models sensitized these cells to chemotherapy treatment, but not radiotherapy. The increased sensitivity was completely reversed by the addition of exogeneous GDNF, confirming the key role of this factor in chemoresistance. Finally, a CRISPR KO of GFRA1 demonstrated a similar increased sensitivity to temozolomide and lomustine treatment, as well as radiotherapy. Together, our findings support the role of the GDNF/GFRA1 signaling pathway in glioblastoma chemo and radioresistance.

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BRD4 marks chromatin on cell cycle genes activates their transcription and orchestrates mitotic cell division

Project description:BRD4 marks chromatin on cell cycle genes activates their transcription and orchestrates mitotic cell division

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