{"database":"ENA","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Fastqsanger.gz":["ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR296/067/SRR29641467/SRR29641467_2.fastq.gz","ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR296/063/SRR29641463/SRR29641463_1.fastq.gz","ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR296/071/SRR29641471/SRR29641471_1.fastq.gz","ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR296/065/SRR29641465/SRR29641465_1.fastq.gz","ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR296/063/SRR29641463/SRR29641463_2.fastq.gz","ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR296/069/SRR29641469/SRR29641469_2.fastq.gz","ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR296/073/SRR29641473/SRR29641473_1.fastq.gz","ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR296/071/SRR29641471/SRR29641471_2.fastq.gz","ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR296/065/SRR29641465/SRR29641465_2.fastq.gz","ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR296/064/SRR29641464/SRR29641464_1.fastq.gz","ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR296/067/SRR29641467/SRR29641467_1.fastq.gz","ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR296/062/SRR29641462/SRR29641462_2.fastq.gz","ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR296/068/SRR29641468/SRR29641468_2.fastq.gz","ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR296/070/SRR29641470/SRR29641470_1.fastq.gz","ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR296/072/SRR29641472/SRR29641472_2.fastq.gz","ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR296/062/SRR29641462/SRR29641462_1.fastq.gz","ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR296/066/SRR29641466/SRR29641466_2.fastq.gz","ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR296/068/SRR29641468/SRR29641468_1.fastq.gz","ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR296/066/SRR29641466/SRR29641466_1.fastq.gz","ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR296/064/SRR29641464/SRR29641464_2.fastq.gz","ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR296/069/SRR29641469/SRR29641469_1.fastq.gz","ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR296/073/SRR29641473/SRR29641473_2.fastq.gz","ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR296/072/SRR29641472/SRR29641472_1.fastq.gz","ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR296/070/SRR29641470/SRR29641470_2.fastq.gz"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Genomics"],"center_name":["University of Illinois Urbana-Champaign"],"full_dataset_link":["https://www.ebi.ac.uk/ena/browser/view/PRJNA1129517"],"scientific_name":["Homo sapiens"],"long_description":["RNA polymerase III (Pol III) activity in cancer is linked to the production of small noncoding (nc)RNAs that are otherwise silent in most tissues. snaR-A (small NF90-associated RNA isoform A) - a hominid-specific ncRNA shown to enhance cell proliferation, migration, and invasion - is a cancer-emergent Pol III product that remains largely uncharacterized despite promoting growth phenotypes. Here, we applied a combination of genomic and biochemical approaches to predict the biogenesis and subsequent protein interactions of snaR-A to better understand its role as a putative driver of cancer progression. By profiling the chromatin landscapes across a multitude of primary tumor types, we show that predicted snaR-A upregulation is broadly linked with unfavorable outcomes among cancer patients. At the molecular level, we unexpectedly discover widespread interactions between snaR-A and mRNA splicing factors, including SF3B2 - a core component of the U2 small nuclear ribonucleoprotein (snRNP). We find that SF3B2 levels are sensitive to high snaR-A abundance, and that depletion of snaR-A alone is sufficient to decrease intron retention levels across subpopulations of mRNA enriched for U2 snRNP occupancy. snaR-A sensitive genes are characterized by high GC content, close spatial proximity to nuclear bodies concentrated in pre-mRNA splicing factors, and functionally enriched for proteins involved in deacetylation and autophagy. We highlight examples of splicing resolution and increased protein levels following snaR-A depletion for a wide-ranging set of factors, suggesting snaR-A-driven splicing defects may have far-reaching effects that re-shape the cellular proteome. These findings help clarify the molecular activities and consequences of snaR-A express- ion in cancer, and altogether establish a novel mechanism through which Pol III overactivity may promote tumorigenesis. Overall design: To investigate the effect of snaR-A on splicing of mRNAs, we performed snaR-A knockdown using three different siRNAs targeting snaR-A in HEK293T cells and deep sequenced the samples. The experiment included three biological replicates for both the scramble knockdown and the snaR-A knockdown. Raw mRNA signal counts were extracted."],"tag":["xref:PubMed:39005375"],"repository":["ENA"],"additional_accession":[]},"is_claimable":false,"name":"Cancer-associated snaR-A noncoding RNA interacts with core splicing machinery and disrupts processing of mRNA subpopulations","description":"Cancer-associated snaR-A noncoding RNA interacts with core splicing machinery and disrupts processing of mRNA subpopulations","dates":{"last_updated":"2025-09-24","first_public":"2024-07-28"},"accession":"PRJNA1129517","cross_references":{"GEO":["GSE271057"],"taxon":["9606"],"PubMed":["39005375"]}}