NSUN2 regulates thyroid cancer-associated alternative splicing switches
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1024963 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR26304211_1.fastq.gz | Fastqsanger.gz | |||
| SRR26304211_2.fastq.gz | Fastqsanger.gz | |||
| SRR26304212_1.fastq.gz | Fastqsanger.gz | |||
| SRR26304212_2.fastq.gz | Fastqsanger.gz | |||
| SRR26304213_1.fastq.gz | Fastqsanger.gz |
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Project description:In this research, we find that both m5C deposition in splice site boundaries and in splicing, direct AS switches of specific thyroid cancer- associated transcripts. We also show that several of the AS events validated in vitro are associated with a poor overall survival rate for patients with thyroid cancer, suggesting the use of these AS events as a novel potential prognostic biomarker.
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Project description:Differentiating erythroid cells execute a unique gene expression program that insures synthesis of the appropriate proteome at each stage of maturation. Standard expression microarrays provide important insight into erythroid gene expression, but cannot detect qualitative changes in transcript structure, mediated by RNA processing, that alter structure and function of encoded proteins. We analyzed stage-specific changes in the late erythroid transcriptome via use of high resolution microarrays that detect altered expression of individual exons. Ten differentiation-associated changes in erythroblast splicing patterns were identified, including the previously known activation of protein 4.1R exon 16 splicing. Six new alternative splicing switches involving enhanced inclusion of internal cassette exons were discovered, as well as three changes in use of alternative first exons. All of these erythroid stage-specific splicing events represent activated inclusion of authentic annotated exons, suggesting they represent an active regulatory process rather than a general loss of splicing fidelity. The observation that three of the regulated transcripts encode RNA binding proteins (SNRP70, HNRPLL, MBNL2) may indicate significant changes in the RNA processing machinery of late erythroblasts. Together these results support the existence of a regulated alternative pre-mRNA splicing program that is critical for late erythroid differentiation. Keywords: Time course; Splicing-sensitive microarray For Exon array hybridizations: 3 biological replicates of day 7, 2 biological replicates of day 10, 3 biological replicates of day 14; For HJAY array hybridizations: 5 biological replicates each were analyzed from day 7 and day 14. One day 14 replicate was deemed an outlier and removed from subsequent analyses.
2010-05-16 | E-GEOD-14588 | biostudies-arrayexpress
Project description:Differentiating erythroid cells execute a unique gene expression program that insures synthesis of the appropriate proteome at each stage of maturation. Standard expression microarrays provide important insight into erythroid gene expression, but cannot detect qualitative changes in transcript structure, mediated by RNA processing, that alter structure and function of encoded proteins. We analyzed stage-specific changes in the late erythroid transcriptome via use of high resolution microarrays that detect altered expression of individual exons. Ten differentiation-associated changes in erythroblast splicing patterns were identified, including the previously known activation of protein 4.1R exon 16 splicing. Six new alternative splicing switches involving enhanced inclusion of internal cassette exons were discovered, as well as three changes in use of alternative first exons. All of these erythroid stage-specific splicing events represent activated inclusion of authentic annotated exons, suggesting they represent an active regulatory process rather than a general loss of splicing fidelity. The observation that three of the regulated transcripts encode RNA binding proteins (SNRP70, HNRPLL, MBNL2) may indicate significant changes in the RNA processing machinery of late erythroblasts. Together these results support the existence of a regulated alternative pre-mRNA splicing program that is critical for late erythroid differentiation. Keywords: Time course; Splicing-sensitive microarray
2009-07-01 | GSE14588 | GEO
Project description:Papillary thyroid cancer (PTC) is often characterized by the indolent behavior with slow cell proliferation, however, small tumors still have a tendency to metastasize to the cervical lymph node, and the molecular mechanisms underlying that remain poorly understood. FN1 is an extracellular matrix (ECM) protein with the controversial role in tumors, containing three alternative splicing domains. In this study, FN1 was as the hottest gene of PTC and distinctive expression in PTC cells. The alternatively splicing EDB region of FN1 was exclusively expressed in tumors, which impacted on integrin β1 (ITGB1) bonding FN1 and it secretion process, resulting in completely distinct roles of two isoforms of FN1 including and skipping EDB domain. EDB(-)FN1 intracellularly inhibited tumor proliferation, whereas extracellular EDB(+)FN1 activated migration, invasion and lymphoangiogenesis in vitro and in vivo. Mechanistically, EDB(-)FN1 upregulated p21 in p53 signaling pathway, however, EDB(+)FN1 secretes into ECM promoted VEGFC expression. Collectively, FN1 is a potential determinant behind the characteristic behavior of PTC with its two isoforms playing distinct roles owing to the alternative splicing of EDB domain.
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Project description:This SuperSeries is composed of the following subset Series: GSE23513: Position-dependent alternative splicing activity revealed by global profiling of alternative splicing events regulated by PTB (HJAY) GSE23514: Position-dependent alternative splicing activity revealed by global profiling of alternative splicing events regulated by PTB (Exon array) Refer to individual Series
2010-09-01 | E-GEOD-23522 | biostudies-arrayexpress
Project description:FN1 Shapes the Behavior of Papillary Thyroid Carcinoma through Alternative Splicing of EDB Region
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Project description:Alternative polyadenylation has been implicated as an important regulator of gene expression. In some cases, alternative polyadenylation is known to couple with alternative splicing to influence last intron removal. However, it is unknown whether alternative polyadenylation events influence alternative splicing decisions at upstream exons. Knockdown of the polyadenylation factors CFIm25 or CstF64 was used as an approach in identifying alternative polyadenylation and alternative splicing events on a genome-wide scale. Although hundreds of alternative splicing events were found to be differentially spliced in the knockdown of CstF64, genes associated with alternative polyadenylation did not exhibit an increased incidence of alternative splicing. These results demonstrate that the coupling between alternative polyadenylation and alternative splicing is usually limited to defining the last exon. The striking influence of CstF64 knockdown on alternative splicing can be explained through its effects on UTR selection of known splicing regulators such as hnRNP A2/B1, thereby indirectly influencing splice site selection. We conclude that changes in the expression of the polyadenylation factor CstF64 influences alternative splicing through indirect effects. HeLa cell line was stably transfected with shRNA plasmids targeting CstF64. Total RNA was isolated from CstF64 KD cells and wild-type control cells using Trizol according to manufacturerâs protocols. Samples were deep sequenced in duplicate using the Illumina GAIIx system.
2016-03-14 | E-GEOD-79157 | biostudies-arrayexpress
Project description:We analyzed alternative splicing with Shh medulloblastoma. This dataset contains bam files of whole genome sequencing from 4 cases. Genomic DNA was isolated from both tumor and matched control specimens. We performed whole genome sequence on Illumina Hiseq.
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Project description:Papillary thyroid cancer (PTC) is an ever-increasing cancer type worldwide, and greatly decreases the life quality and affects survival time of patients during its development and progression, but the underlying mechanisms and key factors for PTC progression are not clear. Recent studies demonstrated the potassium channel protein SK4, also named as KCNN4, participates in the progression of many cancers, while it lacks the molecular mechanism study for SK4 function. In this study, we performed functional and molecular explorations for SK4 by overexpressing its level in thyroid cancer BHT101 cells. Cellular proliferation and invasion experiments were performed to assess the influences of SK4 on cell behaviors. Further, whole transcriptome sequencing (RNA-seq) analysis helped us systematically investigated the down stream targets of SK4, including differentially expressed genes (DEGs) and regulated alternative splicing events (RASEs). We finally validated several DEGs and RASEs associated with the functions of SK4 by RT-qPCR experiment. In thyroid cancer patients, SK4 expression was completely lost in normal tissues and significantly increased in every stage of tumor tissues compared with normal tissues, the reason of which probably results from the low DNA methylation level at its promoter region. Consistent with previous study, SK4 overexpression (SK4-OE) promoted proliferation level and invasion ability of BHT10 cells compared with negative control (NC). By analyzing the RNA-seq data, we detected dozens of DEGs and found that up DEGs were enriched in negative regulation of apoptotic progress, including VTCN1, MSX1, FATE1, TEK, and PRAMEF2. More importantly, we found SK4-OE globally changed the alternative splicing pattern and identified 1639 RASEs. The genes of RASEs were enriched in DNA damage/repair, viral process, translation, and mRNA splicing pathways, which were tightly associated with the pathogenesis and progression of cancers. The splicing regulatory genes from RASGs could partly explain the reason of global AS dysregulation by SK4-OE in BHT101 cells. Finally, we validated several DEGs and RASEs associated with PTC progression by RT-qPCR. We found the expression of VTCN1, EDN1, SLC29A4, RP11-473M20.16, and CH507-513H4.4 were validated by RT-qPCR, as well as the AS pattern of TMEM116, RBM39, and RBM6. In summary, our results deeply explored the molecular targets of SK4 associated them with SK4-induced progression of PTC. We highlight that SE4-regulated AS pattern probably is a novel regulatory mechanism for SK4 in PTC. The identified DEGs and RASEs, as well as SK4 itself, could be used as potential therapeutic targets for PTC treatment in future.
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Project description:Alternative splicing of pre-mRNA is a prominent mechanism to generate protein diversity, yet its regulation is poorly understood. Here, we demonstrate a direct role for histone modifications in alternative splicing. We find distinctive histone modification signatures which correlate with splicing outcome in a set of human genes. Modulation of histone modifications causes splice site switching. The mechanism for histone-mediated splice site selection involves a histone mark which is read by a chromatin protein, which in turn recruits a splicing regulator. These results outline an adaptor system for reading of histone marks by the pre-mRNA splicing machinery. To obtain an estimate of how many PTB-dependent alternative splicing events are regulated by SET2/MRG15-mediated recruitment of PTB, we carried out a genomewide comparative analysis of alternative splicing in hMSC cells depleted of either SETD2, MRG15 or PTB using specific siRNAs, or mock-depleted using a control siRNA.
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