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Study on the functional mechanism of NOP2 in regulating lung cancer development

ABSTRACT: Study on the functional mechanism of NOP2 in regulating lung cancer development

PROVIDER: PRJNA1126124 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29476315_1.fastq.gz	Fastqsanger.gz
	SRR29476315_2.fastq.gz	Fastqsanger.gz
	SRR29476316_1.fastq.gz	Fastqsanger.gz
	SRR29476316_2.fastq.gz	Fastqsanger.gz
	SRR29476317_1.fastq.gz	Fastqsanger.gz

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Study on the functional mechanism of NOP2 in regulating lung cancer development

Project description:NOP2 is a member of the NOL1/NOP2/SUN structural domain (NSUN) family and is responsible for catalyzing post-transcriptional modification of RNA via 5-methylcytosine (m5C). m5C modification dysregulation has been implicated in the pathogenesis of a variety of malignancies. Here, we investigated the expression of NOP2 in lung cancer tissues and cells and found that its expression was significantly upregulated. This is consistent with previous reports. To further investigate the mechanism by which NOP2 affects lung cancer development, RNA sequence analysis was performed. In conclusion, our study emphasizes the important role of NOP2 in lung cancer, and its promise as a potential target for lung cancer therapy.

2024-06-20 | GSE270282 | GEO

Genome-wide miCLIP-Seq reveals methylation targets and RNA interactome of human NOP2/NSUN1

Project description:5-Methylcytosine (m5C) is a base modification broadly found on a variety on coding and non-coding RNAs in the human transcriptome. In eukaryotes m5C is catalyzed by enzymes of the NOL1/NOP2/SUN domain (NSUN) family, which is composed of seven members in humans (NSUN1-7). NOP2/NSUN1, a member of this family, has been mostly characterized in budding yeast as an essential ribosome biogenesis factor required for the deposition of m5C at position C2870 of the 25S rRNA. Although human NOP2/NSUN1 has been known to be an oncogene overexpressed in several types of cancer for decades, its functions remain poorly characterized. To better define the roles of NOP2/NSUN1 in human cells, we used an adapted genome-wide methylation of individual-nucleotide-resolution crosslinking and immunoprecipitation-sequencing (miCLIP-seq) approach to identify its RNA methylation targets. Our analysis revealed that vault RNA 1.2 (vtRNA1.2) and 28S rRNA are NOP2/NSUN1-specific methylated targets. In addition, NOP2/NSUN1 predominantly binds to rRNA, followed by C/D box snoRNA, and other ncRNAs. Together, our data provided a genome-wide spectrum of NOP2/NSUN1 binding RNA and methylated target RNA for understanding the function of human NOP2/NSUN1.

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Methionine metabolism and NOP2 methyltransferase are essential for MYC-Driven liver tumorigenesis

Project description:Hepatocellular carcinoma (HCC) represents the third leading cause of cancer-related death worldwide and has been increasing in recent years in developed nations.1,2 The MYC oncogene or its paralogs are frequently amplified or overexpressed in particularly aggressive subtypes of cancer associated with stem cell-like features and worse clinical outcomes,3,4 including in liver cancer.5 Unfortunately, selective inhibitors that target MYC or its transcriptional program are not yet clinically available for therapy of HCC. Here, we identified methionine metabolism as a selective vulnerability for MYC but not RAS-driven liver cancers. MYC-driven liver cancer cells are methionine dependent and S-adenosylmethionine (SAM), the predominant methyl donor, partially rescues methionine depletion. A low methionine diet, or the methylation inhibitor 5-azacytidine limited MYC-driven tumor formation, but RAS-driven liver cancer was resistant to a low methionine diet. Metabolic tracing of methionine catabolism in MYC high cells identified increased m5C methylation of genomic DNA or ribosomal RNA. We found NOP2, an rRNA m5C-methyltransferase, was regulated by both MYC and methionine. RNA bisulfite seq demonstrated that methionine depletion reduced methylation levels at 28S rRNA C4099, C3438 and C3683. NOP2 knockdown decreased the methylation at C4099, and slightly affected C3438 methylation, suggesting the involvement of NOP2 in methionine dependence. Depletion of NOP2 selectively inhibited MYC liver cancer cell proliferation, tumorigenesis and in vivo tumor growth. Thus, methionine catabolism is critical for MYC-driven liver tumorigenesis and NOP2 may serve as a new therapeutic target in liver cancer.

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