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Credentialling a c-MYC-driven genetic neuroblastoma model [RNAseq-NB]

ABSTRACT: Credentialling a c-MYC-driven genetic neuroblastoma model [RNAseq-NB]

PROVIDER: PRJNA1073948 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27892056_1.fastq.gz	Fastqsanger.gz
	SRR27892056_2.fastq.gz	Fastqsanger.gz
	SRR27892057_1.fastq.gz	Fastqsanger.gz
	SRR27892057_2.fastq.gz	Fastqsanger.gz
	SRR27892058_1.fastq.gz	Fastqsanger.gz

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Credentialling a c-MYC-driven genetic neuroblastoma model [RNAseq-NB]

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Project description:High-risk neuroblastoma (NB) often involves amplification of the neural MYC (MYCN) oncogene as well as mutations in ALK. Currently, high-risk NB presents significant clinical challenges, and additional therapeutic options are needed. Oncogenes such as MYCN and ALK result in increased replication stress in cancer cells, offering one such therapeutically exploitable option. Here, we followed up on earlier phosphoproteomic analyses that identified ATR activity in ALK-driven NB cell lines. We tested several ATR inhibitors, identifying BAY 1895344 as the most potent inhibitor of NB cell growth and proliferation. Using RNA-Seq, proteomics and phosphoproteomics we characterized the response of NB cells and tumours to ATR inhibition, identifying key components of the DNA damage response (DDR) as well as ATRX, MYCN, E2F and DCK among other ATR targets in NB cells. ATR inhibition with BAY 1895344 also produced robust responses in mouse NB models. Remarkably, a 2 week protocol combining ATR and ALK inhibition led to complete regression of NB tumours in two independent NB genetically modified mouse tumour models. These results suggest that NB patients, particularly in high-risk groups with oncogene induced replication stress, may benefit from inhibition of ATR as therapeutic intervention.

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Project description:ALK is a tyrosine kinase receptor and oncogene in neuroblastoma (NB). The receptor is activated by the ALKAL2 ligand, but it is unknown whether missregulation of this ligand may play a role in NB carcinogenesis. Here, a TH-MYCN driven neuroblastoma mice was created +/- ALK F1178S mutation and +/- ALKAL2 overexpression

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Project description:Credentialling a c-MYC–driven genetic neuroblastoma model for pre-clinical studies

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Project description:To elucidate potential role of piRNAs in Neuroblastoma (NB), we performed the genome wide profiling in two human NB cell lines, IMR-32 and SH-SY-5Y by adopting high-throughput RNA sequencing (RNA-Seq) and unveil their possible functions in neoplastic pathways. The RNA sequencing results revealed both known and novel piRNAs in both the cell lines. We observed a total 630 annotated mature piRNAs, distributed across chromosomes and mitochondria which were mapped to various genomic locations such as introns, protein coding regions, repeats, pseudogenes, ncRNAs etc. This is the first study reporting the extensive catalogue of human NB piRNAs which will provide a useful resource to dissect complex neoplastic events that are possibly mediated by piRNAs in neuroblastoma. Moreover, these piRNAs could be used as probable small RNA biomarkers for the Neuroblastoma.

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Project description:Neuroblastoma (NB) is a paediatric tumor wherein amplification of the oncogenic basic helix-loop-helix (bHLH) transcription factor (TF) MYCN confers clinical and biologic features prototypical of Myc-dependent cancers. TF-dependent cancers like MYCN-amplified NB are difficult to target, but the availability of clinical-candidate transcription inhibitors makes selective blockade of oncogenic TF activity a possibility. Here we investigated whether NB could be controlled via dual targeting of the transcription elongation machinery and cell cycle progression, using an orally bioavailable and selective CDK9/2 inhibitor CYC065. CYC065 blocks nascent transcription and leads to a drastic reduction in steady-state levels of short-lived transcripts. In MYCN-amplified NB, CYC065 rapidly and completely eliminated MYCN mRNA and protein, terminating expression of a MYCN-dependent gene expression programme. This result is phenocopied by multiple clinical-candidate CDK9 chemical inhibitors and genetic manipulation of CDK9. Mechanistically, CYC065 dissociates MYCN from physical proximity of P-TEFb in cells. P-TEFb co-occupies promoters and enhancers of de-differentiating pathway genes highly-occupied by MYCN, and CDK9 inhibition terminates expression of these and other highly transcribed genes. Intriguingly, targeted inhibition of CDK9 alone is insufficient to eradicate MYCN-dependent cells lines as CDK9 loss alone is compensated by upregulation of CDK2. CYC065 targeted MYCN-driven neuroblastoma in vivo, resulted in tumor regression or eradication and prolonged survival in multiple NB models, and was effective against a wide range of Myc-dependent cancer cells lines in vitro. The data establish that combined CDK9/CDK2 inhibition blocks transcriptional dependence induced by MYCN, highlighting a potential clinical strategy by which many Myc-driven cancers could be targeted.

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