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Aberrant hyperediting of myeloma transcriptome by ADAR1 confers oncogenicity and is a marker of poor prognosis

ABSTRACT: Aberrant hyperediting of myeloma transcriptome by ADAR1 confers oncogenicity and is a marker of poor prognosis

PROVIDER: PRJNA433846 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6710120_1.fastq.gz	Fastqsanger.gz
	SRR6710120_2.fastq.gz	Fastqsanger.gz
	SRR6710130_1.fastq.gz	Fastqsanger.gz
	SRR6710130_2.fastq.gz	Fastqsanger.gz
	SRR6710121_1.fastq.gz	Fastqsanger.gz

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Aberrant hyperediting of myeloma transcriptome by ADAR1 confers oncogenicity and is a marker of poor prognosis

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Project description:The introduction of new therapies against particular genetic mutations in non-small cell lung cancer is a promising avenue for improving the survival of these patients, but the target population is small. There is a need to uncover new potential actionable genetic lesions and non-conventional cancer pathways, such as RNA editing, are worthy to explore. Herein we show that the adenosine-to-inosine editing enzyme ADAR1 undergoes gene amplification in non-small cancer cell lines and primary tumors in association with higher levels of the corresponding mRNA and protein. From a growth and invasion standpoint, the depletion of ADAR1 expression in amplified cells reduces their tumorigenic potential in cell culture and mice models, whereas its overexpression causes the opposite effects. From a functional perspective, ADAR1 overexpression enhances the editing frequencies of target transcripts such as NEIL1 and miR-381. In the clinical setting, patients with early stage lung cancer, but harboring ADAR1 gene amplification, show poor outcome. Overall, our results indicate a role for ADAR1 as a lung cancer oncogene undergoing gene amplification-associated activation that affect downstream RNA editing patterns and patient prognosis.

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Project description:Multiple myeloma is a malignancy of antibody-secreting plasma cells. Most patients benefit from current therapies, however, 20% of patients relapse or die within two years. To better understand and identify these ‘high-risk’ cases, we analyzed the translocation landscape of myeloma from 795 newly-diagnosed patients by whole genome sequencing from the CoMMpass study. Translocations involving the immunoglobulin lambda (IgL) locus were identified in 10% of patients, and were indicative of poor prognosis. Importantly, 70% of IgL translocations co-occurred with hyperdiploid disease, a marker of standard risk, potentially resulting in the misclassification of IgL-translocated myeloma. Most IgL-translocations coincided with focal amplifications that were centered on the 3’ enhancer. Patients with IgL-translocations failed to benefit from immunomodulatory imide drugs (IMiDs), which target the lymphocyte-specific transcription factor IKZF1 that is bound to the IgL 3’ enhancer at some of the highest levels in the myeloma epigenome. These data implicate IgL-translocation as a driver of poor prognosis which may be due in part to IMID resistance.

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