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RNA editing modulates pathways critical to B cell lymphomagenesis

ABSTRACT: RNA editing modulates pathways critical to B cell lymphomagenesis

PROVIDER: PRJNA605715 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11050913_1.fastq.gz	Fastqsanger.gz
	SRR11050913_2.fastq.gz	Fastqsanger.gz
	SRR11050914_1.fastq.gz	Fastqsanger.gz
	SRR11050914_2.fastq.gz	Fastqsanger.gz
	SRR11050915_1.fastq.gz	Fastqsanger.gz

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RNA editing modulates pathways critical to B cell lymphomagenesis

Project description:Diffuse large B cell lymphoma (DLBCL) is one of the most common and aggressive types of B cell lymphoma. Subtype heterogeneity cannot be completely explained by genomic alterations and/or gene expression differences, suggesting that additional mechanisms are involved. Here, we explore the contribution of an epitranscriptomic modification to B cell lymphomagenesis. Our data demonstrate that ADAR1-mediated RNA editing (deamination of adenosine to inosine) targets novel candidate driver genes within well-known disease-associated pathways in DLBCL. Within these pathways, DNA mutations and RNA editing events are often mutually exclusive at the gene level, suggesting that tumours can modulate pathway outcomes by altering sequence at either the genomic or the transcriptomic level. In contrast to what has been found in solid tumours, in DLBCL low ADAR1 expression correlates with low interferon-stimulated gene (ISG) scores and with a microenvironment that is not inflamed. To investigate the molecular mechanism behind the inability of DLBCL to mount an ISG response upon loss of ADAR1, we focused on one candidate MAVS, a central regulator of ISG (as well as NFkB) signaling. MAVS is never mutated but robustly edited by ADAR1 at its 3’UTR, and editing correlates with increased MAVS protein levels and increased downstream activation of the ISG as well as NFkB pathways. Using targeted base editing tools to specifically restore MAVS editing in ADAR1-deficient cells, we demonstrate that MAVS editing is directly causal to an increase in expression of genes downstream this signaling pathway. Our data imply that DLBCL tumours edit MAVS to strengthen NFkB signaling, to which they are dependent on survival; thus, targeted loss of MAVS editing might sensitize tumours to cell death. Overall, ADAR1-mediated RNA editing represents a new tumour evasion mechanism underlying DLBCL lymphomagenesis, with features distinct from those derived from solid tumours to date.

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Project description:The project aims to evaluate the contribution of ADAR1 RNA editing to B cell lymphomagenesis, specifically in diffuse large B cell lymphoma (DLBCL). Within our DLBCL cohort, RNA editing targets transcripts within known lymphoma-driving pathways such as apoptosis, p53 and NF-kB signaling, as well as the previously unrecognized RIG-I-like pathway. In the latter context, we show that ADAR1-mediated editing in the MAVS transcript correlates with increased MAVS protein expression levels, associating with increased interferon/NF-kB signaling and increased T cell exhaustion. To confirm this mechanism, we have performed LC-MSMS analysis on a DLBCL cell line (RCK8) in the presence or absence of ADAR1 (Figure S11D ). Additionally, using targeted RNA base editing tools to restore editing within MAVS 3'UTR in ADAR1-deficient cells, we demonstrate that editing is likely to be causal to an increase in downstream signaling in the absence of activation by canonical nucleic acid receptor sensing. To confirm that this signaling increase depends on an increase of MAVS protein upon specific editing, we have performed LC-MSMS analysis on the same samples (Figure 4G).

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