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LINE-associated cryptic splicing induces dsRNA-mediated interferon response and tumor immunity [RNA-seq]

ABSTRACT: LINE-associated cryptic splicing induces dsRNA-mediated interferon response and tumor immunity [RNA-seq]

PROVIDER: PRJNA942955 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23782851_1.fastq.gz	Fastqsanger.gz
	SRR23782851_2.fastq.gz	Fastqsanger.gz
	SRR23782852_1.fastq.gz	Fastqsanger.gz
	SRR23782852_2.fastq.gz	Fastqsanger.gz
	SRR23782853_1.fastq.gz	Fastqsanger.gz

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LINE-associated cryptic splicing induces dsRNA-mediated interferon response and tumor immunity

Project description:LINE-associated cryptic splicing induces dsRNA-mediated interferon response and tumor immunity

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LINE-associated cryptic splicing induces dsRNA-mediated interferon response and tumor immunity [iCLIP]

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LINE-associated cryptic splicing induces dsRNA-mediated interferon response and tumor immunity [iCLIP]

Project description:RNA splicing plays a critical role in post-transcriptional gene regulation. Exponential expansion of intron length poses a challenge for accurate splicing. Little is known about how cells prevent inadvertent and often deleterious expression of intronic elements due to cryptic splicing. In this study, we identify hnRNPM as an essential RNA binding protein that suppresses cryptic splicing through binding to deep introns, preserving transcriptome integrity. Long interspersed nuclear elements (LINEs) harbor large amounts of pseudo splice sites in introns. hnRNPM preferentially binds at intronic LINEs and represses LINE-containing pseudo splice site usage for cryptic splicing. Remarkably, a subgroup of the cryptic exons can form long dsRNAs through base-pairing of inverted Alu transposable elements scattered in between LINEs and trigger interferon immune response, a well-known antiviral defense mechanism. Notably, these interferon-associated pathways are found to be upregulated in hnRNPM-deficient tumors, which also exhibit elevated immune cell infiltration. These findings unveil hnRNPM as a guardian of transcriptome integrity. Targeting hnRNPM in tumors may be used to trigger an inflammatory immune response thereby boosting cancer surveillance.

2024-05-29 | GSE227048 | GEO

LINE-associated cryptic splicing induces dsRNA-mediated interferon response and tumor immunity [RNA-seq]

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LINE-associated cryptic splicing induces dsRNA-mediated interferon response and tumor immunity

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-05-29 | GSE227050 | GEO

Whole blood transcriptome alteration between pigs with extreme in vivo dsRNA-induced serum interferon-alpha production

Project description:The interferon (IFN) is a major effector of the innate immunity which mediates an adaptive immune response against broad spectrum pathogens. The aim of this work has been to investigate the differences of the virus mimic dsRNA (Poly I:C)-inducted in vivo transcriptomic alteration between pigs with high (HIGH) and low (LOW) serum interferon-alpha production. The pigs with extreme yield of induced interferon-alpha from a F2 resource population were selected for whole blood gene expression analysis using the porcine Affymetrix microarray

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Function of HNRNPC in breast cancer cells by controlling the dsRNA-induced interferon response

Project description:Elevated expression of RNA binding protein HNRNPC has been reported in cancer cells, while the essentialness and functions of HNRNPC in tumors were not clear. We showed that repression of HNRNPC in the breast cancer cells MCF7 and T47D inhibited cell proliferation and tumor growth. Our computational inference of the key pathways and extensive experimental investigations revealed that the cascade of interferon responses mediated by RIG-I was responsible for such tumor-inhibitory effect. Interestingly, repression of HNRNPC resulted in accumulation of endogenous double-stranded RNA (dsRNA), the binding ligand of RIG-I. These up-regulated dsRNA species were highly enriched by Alu sequences and mostly originated from pre-mRNA introns that harbor the known HNRNPC binding sites. Such source of dsRNA is different than the recently well-characterized endogenous retroviruses that encode dsRNA. In summary, essentialness of HNRNPC in the breast cancer cells was attributed to its function in controlling the endogenous dsRNA and the down-stream interferon response. This is a novel extension from the previous understandings about HNRNPC in binding with introns and regulating RNA splicing.

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Enhancer decommissioning by MLL4 ablation elicits dsRNA-interferon signaling and GSDMD-mediated pyroptosis to potentiate anti-tumor immunity

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Inhibition of METTL3 results in a cell-intrinsic interferon response that enhances anti-tumour immunity [CRISPR screen]

Project description:Therapies that enhance antitumor immunity have altered the natural history of many cancers. Consequently, leveraging nonoverlapping mechanisms to increase immunogenicity of cancer cells remains a priority. Using a novel enzymatic inhibitor of the RNA methyl-transferase METTL3, we demonstrate a global decrease in N6-methyladenosine (m6A) results in double-stranded RNA (dsRNA) formation and a profound cell-intrinsic interferon response. Through unbiased CRISPR screens, we establish dsRNA-sensing and interferon signaling are primary mediators that potentiate T-cell killing of cancer cells following METTL3 inhibition. We show in a range of immunocompetent mouse models that although METTL3 inhibition is equally efficacious to anti-PD-1 therapy, the combination has far greater preclinical activity. Using SPLINTR barcoding, we demonstrate that anti-PD-1 therapy and METTL3 inhibition target distinct malignant clones, and the combination of these therapies overcomes clones insensitive to the single agents. These data provide the mole-cular and preclinical rationale for employing METTL3 inhibitors to promote antitumor immunity in the clinic.

2023-11-04 | GSE246837 | GEO

Inhibition of METTL3 Results in a Cell-Intrinsic Interferon Response That Enhances Antitumor Immunity [ONT direct RNA-seq]

Project description:Therapies that enhance antitumor immunity have altered the natural history of many cancers. Consequently, leveraging nonoverlapping mechanisms to increase immunogenicity of cancer cells remains a priority. Using a novel enzymatic inhibitor of the RNA methyltransferase METTL3, we demonstrate a global decrease in N6-methyladenosine (m6A) results in double-stranded RNA (dsRNA) formation and a profound cell-intrinsic interferon response. Through unbiased CRISPR screens, we establish dsRNA-sensing and interferon signaling are primary mediators that potentiate T-cell killing of cancer cells following METTL3 inhibition. We show in a range of immunocompetent mouse models that although METTL3 inhibition is equally efficacious to anti–PD-1 therapy, the combination has far greater preclinical activity. Using SPLINTR barcoding, we demonstrate that anti–PD-1 therapy and METTL3 inhibition target distinct malignant clones, and the combination of these therapies overcomes clones insensitive to the single agents. These data provide the molecular and preclinical rationale for employing METTL3 inhibitors to promote antitumor immunity in the clinic.

2024-01-06 | GSE252537 | GEO

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