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The oncogenic circular RNA circ_63706 is a potential therapeutic target in sonic hedgehog-subtype childhood medulloblastomas.

ABSTRACT: The oncogenic circular RNA circ_63706 is a potential therapeutic target in sonic hedgehog-subtype childhood medulloblastomas.

PROVIDER: PRJNA894971 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22064344_1.fastq.gz	Fastqsanger.gz
	SRR22064344_2.fastq.gz	Fastqsanger.gz
	SRR22064345_1.fastq.gz	Fastqsanger.gz
	SRR22064345_2.fastq.gz	Fastqsanger.gz
	SRR22064346_1.fastq.gz	Fastqsanger.gz

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Sonic Hedgehog subgroup medulloblastomas

Project description:Sonic Hedgehog subgroup medulloblastomas

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The oncogenic circular RNA circ_63706 is a potential therapeutic target in sonic hedgehog-subtype childhood medulloblastomas.

Project description:Medulloblastoma (MB) develops through various genetic, epigenetic, and non-coding (nc) RNA-related mechanisms, but the roles played by ncRNAs, particularly circular RNAs (circRNAs), remain poorly defined. CircRNAs are increasingly recognized as stable non-coding RNA therapeutic targets in many cancers, but little is known about their function in MBs. To determine medulloblastoma subgroup-specific circRNAs, publicly available RNA sequencing (RNA-seq) data from 175 MB patients were interrogated to identify circRNAs that differentiate between MB subgroups. circ_63706 was identified as sonic hedgehog (SHH) group-specific, with its expression confirmed by RNA-FISH analysis in clinical tissue samples. The oncogenic function of circ_63706 was characterized in vitro and in vivo. Further, circ_63706-depleted cells were subjected to RNA-seq and lipid profiling to identify its molecular function. Finally, we mapped the circ_63706 secondary structure using an advanced random forest classification model and modeled a 3D structure to identify its interacting miRNA partner molecules. Circ_63706 regulates independently of the host coding gene pericentrin (PCNT), and its expression is specific to the SHH subgroup. circ_63706-deleted cells implanted into mice produced smaller tumors, and mice lived longer than parental cell implants. At the molecular level, circ_63706-deleted cells elevated total ceramide and oxidized lipids and reduced total triglyceride. Our study implicates a novel oncogenic circular RNA in the SHH medulloblastoma subgroup and establishes its molecular function and potential as a future therapeutic target.

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The miR-17/92 Polycistron Is Up-regulated in Sonic Hedgehog-Driven Medulloblastomas and Induced by N-myc in Sonic Hedgehog–Treated Cerebellar Neural Precursors

Project description:Medulloblastoma is the most common malignant pediatric brain tumor, and mechanisms underlying its development are poorly understood. We identified recurrent amplification of the miR-17/92 polycistron proto-oncogene in 6% of pediatric medulloblastomas by high-resolution single-nucleotide polymorphism genotyping arrays and subsequent interphase fluorescence in situ hybridization on a human medulloblastoma tissue microarray. Profiling the expression of 427 mature microRNAs (miRNA) in a series of 90 primary human medulloblastomas revealed that components of the miR-17/92 polycistron are the most highly up-regulated miRNAs in medulloblastoma. Expression of miR-17/92 was highest in the subgroup of medulloblastomas associated with activation of the sonic hedgehog (Shh) signaling pathway compared with other subgroups of medulloblastoma. Medulloblastomas in which miR-17/92 was up-regulated also had elevated levels of MYC/MYCN expression. Consistent with its regulation by Shh, we observed that Shh treatment of primary cerebellar granule neuron precursors (CGNP), proposed cells of origin for the Shh-associated medulloblastomas, resulted in increased miR-17/92 expression. In CGNPs, the Shh effector N-myc, but not Gli1, induced miR-17/92 expression. Ectopic miR-17/92 expression in CGNPs synergized with exogenous Shh to increase proliferation and also enabled them to proliferate in the absence of Shh. We conclude that miR-17/92 is a positive effector of Shh-mediated proliferation and that aberrant expression/amplification of this miR confers a growth advantage to medulloblastomas.

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The oncogenic circular RNA circ_63706 is a potential therapeutic target in sonic hedgehog-subtype childhood medulloblastomas.

Project description:To gain further insights into the functional significance of circ_63706, gene expression was measured by RNA-seq in DAOY cells treated with either si-NC (non-targeting control) or si-circ_63706.

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Project description:The causative role of activated Hedgehog signaling in liver fibrosis was investigated in vivo. Using hydrodynamics-based transfection, a transgenic mouse model has been developed that expresses Sonic Hedgehog (SHH), a ligand for Hedgehog signaling, in the liver. Levels of hepatic fibrosis and fibrosis-related gene expression were assessed in the model.

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Molecular mechanisms underlying the development of Sonic Hedgehog subtype medulloblastoma

Project description:Medulloblastoma (MB) is a highly malignant primary brain tumor that originates from the cerebellar granule neuron precursors (CGNPs) in the cerebellum or posterior fossa. The overactivation of the Sonic Hedgehog (Shh) signal pathway accounts for the occurrence of 30% clinical cases of MB. Shh engagement with the inhibitory receptor Patched 1 derepresses the second receptor, Smoothened (Smo), and thereby activates the Gli transcriptional factors, allowing for the expression of a cohort of genes involved in cell growth and differentiation. Nevertheless, the mechanisms of Shh signaling-driven carcinogenesis, e.g. the Gli target genes that play pivotal roles in the transformation of CGNPs, remain largely unknown. To screen for the genes involved in the development of Shh subtype MB, we attempt to analyze genes differentially expressed between CGNPs and MB cells, which will hopefully provide clues for the elucidation of key molecular events that mediate the onset of this specific type of nervous system malignancy.

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