Abstract
U1 small nuclear RNA (U1 snRNA), as one of the most abundant ncRNAs in human cells, plays an important role in splicing of pre-mRNAs. Compared to previous studies which have focused on the primary function of U1 snRNA and the neurodegenerative diseases caused by abnormalities of U1 snRNA, this study is to investigate how U1 snRNA over-expression affects the expression of mammal genes on a genome-wide scale. By comparing the gene expression profiles of U1 snRNA over-expressed cells with those of their controls using microarray experiments, 916 genes or loci were identified significantly Differentially Expressed (DE). These 595 up-regulated DE genes and 321 down-regulated DE genes were analyzed using annotations from GO categories and pathways from the KEGG database. As a result, three of 12 enriched pathways were well-known cancer pathways, while the other nine pathways were associated to cancers in previous studies. The further analysis of 73 genes involved in 12 pathways suggested that U1 snRNA could regulate cancer gene expression. The microarray data under the GEO Series accession number GSE84304 is available in the NCBI GEO database.
Highlights
U1 small nuclear RNA (U1 snRNA) is one of the most abundant ncRNAs [1]
Compared to previous studies which have focused on the primary function of U1 snRNA and the neurodegenerative diseases caused by abnormalities of U1 snRNA, this study is to investigate how U1 snRNA over-expression affects the expression of mammal genes on a genome-wide scale
Bai et al demonstrated that cytoplasmic aggregation www.impactjournals.com/oncotarget of U1 snRNA and U1 snRNPs resulted in a loss of nuclear spliceosome activity, which altered the expression of Amyloid Precursor Protein (APP) and Amyloid Beta (Aβ) protein
Summary
U1 small nuclear RNA (U1 snRNA) is one of the most abundant ncRNAs [1]. U1 snRNA has a length of 164 nt in human and its protein binding sites are highly conserved in insects and mammals [2]. The primary function of U1 snRNA is its involvement in the splicing of pre-mRNAs in nuclei. Abnormalities of U1 snRNA can cause defects in pre-mRNA splicing, which are considered as a primary cause of human diseases [4]. In the year of 2013, Bai et al discovered cytoplasmic aggregation of U1 snRNA with several U1 small nuclear Ribonucleoproteins (U1 snRNPs) in Alzheimer's Disease (AD), but not in other examined neurodegenerative diseases including Parkinson's Disease (PD) and Frontotemporal Lobar Degeneration (FTLD) [5]. Bai et al demonstrated that cytoplasmic aggregation www.impactjournals.com/oncotarget of U1 snRNA and U1 snRNPs resulted in a loss of nuclear spliceosome activity, which altered the expression of Amyloid Precursor Protein (APP) and Amyloid Beta (Aβ) protein. Previous studies concluded that Alternative Splicing (AS) and APA were deregulated and exploited by cancer cells to promote their growth and survival [8], the relationship between expression levels of U1 snRNA and cancers or cancer genes has not been investigated to the best of our knowledge
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