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Transcriptomic Analysis of Gene Networks Regulated by U11 Small Nuclear RNA in Bladder Cancer.

ABSTRACT: Small nuclear RNA is a class of non-coding RNA that widely exist in the nucleus of eukaryotes. Accumulated evidences have shown that small nuclear RNAs are associated with the regulation of gene expression in various tumor types. To explore the gene expression changes and its potential effects mediated by U11 snRNA in bladder cancer cells, U11 snRNA knockout and overexpressed cell lines were constructed and further used to analyze the gene expression changes by RNA sequencing. The differentially expressed genes were found to be mainly enriched in tumor-related pathways both in the U11 knockout and overexpression cell lines, such as NF-kappa B signaling pathway, bladder cancer and PI3K-Akt signaling pathway. Furthermore, alternative splicing events were proposed to participate in the potential regulatory mechanism induced by the U11 knockout or overexpression. In conclusion, U11 may be involved in the regulation of gene expression in bladder cancer cells, which may provide a potentially new biomarker for clinical diagnosis and treatment of bladder cancer.

SUBMITTER: Wang Z

PROVIDER: S-EPMC8283811 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Transcriptomic Analysis of Gene Networks Regulated by U11 Small Nuclear RNA in Bladder Cancer

Project description:U11 may alter gene expression by affecting the PI3K-Akt signaling pathway and NF-kappa B signaling pathway, regulating alternative splicing events of FN1 and RPL22L1, and ultimately leading to the development of bladder cancer.

2021-06-30 | GSE171744 | GEO

Transcriptomic Analysis of Gene Networks Regulated by U11 Small Nuclear RNA in Bladder Cancer

Project description:Transcriptomic Analysis of Gene Networks Regulated by U11 Small Nuclear RNA in Bladder Cancer

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Loss of U11 small nuclear RNA in the developing mouse limb results in micromelia.

Project description:Disruption of the minor spliceosome due to mutations in RNU4ATAC is linked to primordial dwarfism in microcephalic osteodysplastic primordial dwarfism type 1, Roifman syndrome, and Lowry-Wood syndrome. Similarly, primordial dwarfism in domesticated animals is linked to positive selection in minor spliceosome components. Despite being vital for limb development and size regulation, its role remains unexplored. Here, we disrupt minor spliceosome function in the developing mouse limb by ablating one of its essential components, U11 small nuclear RNA, which resulted in micromelia. Notably, earlier loss of U11 corresponded to increased severity. We find that limb size is reduced owing to elevated minor intron retention in minor intron-containing genes that regulate cell cycle. As a result, limb progenitor cells experience delayed prometaphase-to-metaphase transition and prolonged S-phase. Moreover, we observed death of rapidly dividing, distally located progenitors. Despite cell cycle defects and cell death, the spatial expression of key limb patterning genes was maintained. Overall, we show that the minor spliceosome is required for limb development via size control potentially shared in disease and domestication.

| S-EPMC7438004 | biostudies-literature

Additional low-abundance human small nuclear ribonucleoproteins: U11, U12, etc.

Project description:Two-dimensional gel fractionation has revealed the existence of a number (greater than or equal to 8) of additional species of HeLa cell small RNAs that have 5' trimethylguanosine cap structures and are bound by proteins containing Sm epitopes. Therefore, these low-abundance (10(3)-10(4) per cell) RNAs belong to the Sm class of small nuclear ribonucleoproteins (snRNPs), whose best-known members are the four highly abundant (approximately 10(6) per cell) particles required for pre-mRNA splicing. The complexity of Sm snRNPs in mammalian cells is thus not greatly different from that previously established for lower eukaryotes. Two of the new RNAs, designated U11 (131 nucleotides) and U12 (150 nucleotides), have been sequenced. The U11 and U12 snRNPs have been characterized further by examining their nuclease sensitivity and their possible interactions with other snRNPs. Potential roles for the low-abundance snRNPs in aspects of pre-mRNA processing are discussed.

| S-EPMC282611 | biostudies-other

Identification of an evolutionarily divergent U11 small nuclear ribonucleoprotein particle in Drosophila.

Project description:Previous reports suggested that U11, in contrast to U12 or other small nuclear (sn)RNAs of the U12-type spliceosome, might be either highly divergent or absent in Drosophila melanogaster. Affinity purification of Drosophila U12-containing complexes has led to the identification of the fly U11 snRNA, which contains a potential U12-type 5' splice-site-interacting sequence, but whose sequence and length differs significantly from vertebrate and plant U11. Analysis of U12-type introns revealed an A-rich region directly downstream of Drosophila, but not human, U12-type 5' splice sites. This finding, coupled with the presence of a highly divergent U11 snRNA, and the apparent absence of Drosophila homologs of human U11 proteins, suggest that U12-type 5' splice site recognition might be different in flies. A comparison of U11 snRNAs that we have identified from vertebrates, plants, and insects, suggests that an evolutionarily divergent U11 snRNA may be unique to Drosophila and not characteristic of insects in general.

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Coiled bodies preferentially associate with U4, U11, and U12 small nuclear RNA genes in interphase HeLa cells but not with U6 and U7 genes.

Project description:Coiled bodies (CBs) are nuclear organelles involved in the metabolism of small nuclear RNAs (snRNAs) and histone messages. Their structural morphology and molecular composition have been conserved from plants to animals. CBs preferentially and specifically associate with genes that encode U1, U2, and U3 snRNAs as well as the cell cycle-regulated histone loci. A common link among these previously identified CB-associated genes is that they are either clustered or tandemly repeated in the human genome. In an effort to identify additional loci that associate with CBs, we have isolated and mapped the chromosomal locations of genomic clones corresponding to bona fide U4, U6, U7, U11, and U12 snRNA loci. Unlike the clustered U1 and U2 genes, each of these loci encode a single gene, with the exception of the U4 clone, which contains two genes. We next examined the association of these snRNA genes with CBs and found that they colocalized less frequently than their multicopy counterparts. To differentiate a lower level of preferential association from random colocalization, we developed a theoretical model of random colocalization, which yielded expected values for chi2 tests against the experimental data. Certain single-copy snRNA genes (U4, U11, and U12) but not controls were found to significantly (p < 0.000001) associate with CBs. Recent evidence indicates that the interactions between CBs and genes are mediated by nascent transcripts. Taken together, these new results suggest that CB association may be substantially augmented by the increased transcriptional capacity of clustered genes. Possible functional roles for the observed interactions of CBs with snRNA genes are discussed.

| S-EPMC30488 | biostudies-literature

Gene expression profiling of WDR5 regulated genes in bladder cancer.

Project description:WD repeat domain 5 (WDR5) plays an important role in various biological functions through the epigenetic regulation of gene transcription (Wysocka et al., 2005 [1]; Sandstrom et al., 2014[2]; Ang et al., 2011[3]). Recently, our study found that WDR5 was upregulated in bladder cancer tissues, promoted bladder cancer cell proliferation, self-renewal and chemoresistance to cisplatin in bladder cancer cells in vitro, and tumor growth in vivo (Chen et al., 2015). To gain a molecular understanding of the role of WDR5 in promoting bladder cancer, we performed a genome-wide analysis on WDR5 knockdown by microarray gene expression profiling. Here we provide detailed experimental methods and analysis for the microarray data, which have been deposited into Gene Expression Omnibus (GEO): GSE59132.

| S-EPMC4583625 | biostudies-literature

Structural features important for the U12 snRNA binding and minor spliceosome assembly of Arabidopsis U11/U12-small nuclear ribonucleoproteins.

Project description:Although seven proteins unique to U12 intron-specific minor spliceosomes, denoted as U11/U12-65K, -59K, -48K, -35K, -31K, -25K, and -20K, have been identified in humans and the roles of some of them have been demonstrated, the functional role of most of these proteins in plants is not understood. A recent study demonstrated that Arabidopsis U11/U12-65K is essential for U12 intron splicing and normal plant development. However, the structural features and sequence motifs important for 65 K binding to U12 snRNA and other spliceosomal proteins remain unclear. Here, we demonstrated by domain-deletion analysis that the C-terminal region of the 65 K protein bound specifically to the stem-loop III of U12 snRNA, whereas the N-terminal region of the 65 K protein was responsible for interacting with the 59 K protein. Analysis of the interactions between each snRNP protein using yeast two-hybrid analysis and in planta bimolecular fluorescence complementation and luciferase complementation imaging assays demonstrated that the core interactions among the 65 K, 59 K, and 48 K proteins were conserved between plants and animals, and multiple interactions were observed among the U11/U12-snRNP proteins. Taken together, these results reveal that U11/U12-65K is an indispensible component of the minor spliceosome complex by binding to both U11/U12-59K and U12 snRNA, and that multiple interactions among the U11/U12-snRNP proteins are necessary for minor spliceosome assembly.

| S-EPMC4962810 | biostudies-literature

Classifying non-small cell lung cancer types and transcriptomic subtypes using convolutional neural networks.

Project description:ObjectiveNon-small cell lung cancer is a leading cause of cancer death worldwide, and histopathological evaluation plays the primary role in its diagnosis. However, the morphological patterns associated with the molecular subtypes have not been systematically studied. To bridge this gap, we developed a quantitative histopathology analytic framework to identify the types and gene expression subtypes of non-small cell lung cancer objectively.Materials and methodsWe processed whole-slide histopathology images of lung adenocarcinoma (n = 427) and lung squamous cell carcinoma patients (n = 457) in the Cancer Genome Atlas. We built convolutional neural networks to classify histopathology images, evaluated their performance by the areas under the receiver-operating characteristic curves (AUCs), and validated the results in an independent cohort (n = 125).ResultsTo establish neural networks for quantitative image analyses, we first built convolutional neural network models to identify tumor regions from adjacent dense benign tissues (AUCs > 0.935) and recapitulated expert pathologists' diagnosis (AUCs > 0.877), with the results validated in an independent cohort (AUCs = 0.726-0.864). We further demonstrated that quantitative histopathology morphology features identified the major transcriptomic subtypes of both adenocarcinoma and squamous cell carcinoma (P < .01).DiscussionOur study is the first to classify the transcriptomic subtypes of non-small cell lung cancer using fully automated machine learning methods. Our approach does not rely on prior pathology knowledge and can discover novel clinically relevant histopathology patterns objectively. The developed procedure is generalizable to other tumor types or diseases.

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Project description:By means of a computer search for upstream promoter elements (distal sequence element and proximal sequence element) typical of small nuclear RNA genes, we have identified in the human genome a number of previously unrecognized, putative transcription units whose predicted products are novel noncoding RNAs with homology to protein-coding genes. By elucidating the function of one of them, we provide evidence for the existence of a sense/antisense-based gene-regulation network where part of the polymerase III transcriptome could control its polymerase II counterpart.

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