Oncogenic fusions converge on shared mechanisms in initiating astroblastoma [scRNA-seq of Olig2 lineage cells]
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1198591 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR31722565_1.fastq.gz | Fastqsanger.gz | |||
| SRR31722565_2.fastq.gz | Fastqsanger.gz | |||
| SRR31722566_1.fastq.gz | Fastqsanger.gz | |||
| SRR31722566_2.fastq.gz | Fastqsanger.gz | |||
| SRR31722567_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 8 |
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Project description:Chromosomal rearrangements and gene fusions are the initial events in the development of many cancers. Astroblastoma (ABM), a challenging brain cancer of unknown cellular origin, is associated with diverse in-frame gene fusions, including MN1:BEND2 and MN1:CXXC5. However, it remains unclear if these gene fusions contribute to tumorigenesis. Here, we show that the two ABM-associated fusions converge on similar molecular activities and initiate malignancy specifically in ventral telencephalon neural progenitors. BEND2 and CXXC5 recognized similar DNA motifs, suggesting a convergence on downstream gene regulation. Expressing MN1:BEND2 in ventral telencephalon neural progenitors results in aberrant cell proliferation, impaired differentiation, a perivascular occupancy pattern of cells reminiscent of ABM, and acquisition of an ABM-associated transcriptional signature. In stark contrast, MN1:BEND2 expression in dorsal telencephalon neural progenitors leads to extensive cell death. This cell-type specific malignancy is dependent on Olig2 expression. Mechanistically, both ABM-associated fusion proteins (MN1:BEND2 and MN1:CXXC5) induce overlapping transcriptional responses, including the activation of a therapeutically targetable PDGFRα pathway. Collectively, our data suggests that distinct ABM-associated fusions upregulate shared transcriptional networks, thereby disrupting the normal development of ventral telencephalon neural progenitors and culminating in oncogenic transformation. These findings uncover new avenues for targeted ABM treatment.
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Project description:Chromosomal rearrangements and gene fusions are the initial events in the development of many cancers. Astroblastoma (ABM), a challenging brain cancer of unknown cellular origin, is associated with diverse in-frame gene fusions, including MN1:BEND2 and MN1:CXXC5. However, it remains unclear if these gene fusions contribute to tumorigenesis. Here, we show that the two ABM-associated fusions converge on similar molecular activities and initiate malignancy specifically in ventral telencephalon neural progenitors. BEND2 and CXXC5 recognized similar DNA motifs, suggesting a convergence on downstream gene regulation. Expressing MN1:BEND2 in ventral telencephalon neural progenitors results in aberrant cell proliferation, impaired differentiation, a perivascular occupancy pattern of cells reminiscent of ABM, and acquisition of an ABM-associated transcriptional signature. In stark contrast, MN1:BEND2 expression in dorsal telencephalon neural progenitors leads to extensive cell death. This cell-type specific malignancy is dependent on Olig2 expression. Mechanistically, both ABM-associated fusion proteins (MN1:BEND2 and MN1:CXXC5) induce overlapping transcriptional responses, including the activation of a therapeutically targetable PDGFRα pathway. Collectively, our data suggests that distinct ABM-associated fusions upregulate shared transcriptional networks, thereby disrupting the normal development of ventral telencephalon neural progenitors and culminating in oncogenic transformation. These findings uncover new avenues for targeted ABM treatment.
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Project description:Chromosomal rearrangements and gene fusions are the initial events in the development of many cancers. Astroblastoma (ABM), a challenging brain cancer of unknown cellular origin, is associated with diverse in-frame gene fusions, including MN1:BEND2 and MN1:CXXC5. However, it remains unclear if these gene fusions contribute to tumorigenesis. Here, we show that the two ABM-associated fusions converge on similar molecular activities and initiate malignancy specifically in ventral telencephalon neural progenitors. BEND2 and CXXC5 recognized similar DNA motifs, suggesting a convergence on downstream gene regulation. Expressing MN1:BEND2 in ventral telencephalon neural progenitors results in aberrant cell proliferation, impaired differentiation, a perivascular occupancy pattern of cells reminiscent of ABM, and acquisition of an ABM-associated transcriptional signature. In stark contrast, MN1:BEND2 expression in dorsal telencephalon neural progenitors leads to extensive cell death. This cell-type specific malignancy is dependent on Olig2 expression. Mechanistically, both ABM-associated fusion proteins (MN1:BEND2 and MN1:CXXC5) induce overlapping transcriptional responses, including the activation of a therapeutically targetable PDGFRα pathway. Collectively, our data suggests that distinct ABM-associated fusions upregulate shared transcriptional networks, thereby disrupting the normal development of ventral telencephalon neural progenitors and culminating in oncogenic transformation. These findings uncover new avenues for targeted ABM treatment.
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