Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

98 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

CFIm25 links alternative polyadenylation to glioblastoma tumour suppression

ABSTRACT: Purpose: To identify all of the APA targets of CFIm25 on a global scale and develop an algorithm that can idenitify APA events from standard RNA-seq data Methods: RNA from HeLa cells treated with control siRNA and CFIm25 siRNA were subject to RNA-Seq. Using a custom-designed algorithm to mine RNA-seq data for novel APA events regulated by CFIm25. Results: We identified over 1,400 genes with shortened 3’UTRs after CFIm25 knockdown. Importantly, we show that as a consequence of APA, many of these mRNAs have greatly enhanced protein expression due to the loss of destabilizing features within the 3’UTR. Conclusions: Our study underscored the critical function of the CFIm complex members in governing APA and establish a previously unknown link between APA and metabolic pathways important for tumor progression. Hela cell line mRNA profiles of control treated and CFIm25 Knockdown were generated by RNA-Seq using Illumina GAIIx.

ORGANISM(S): Homo sapiens

SUBMITTER: Zheng Xia

PROVIDER: E-GEOD-42420 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Publications

CFIm25 links alternative polyadenylation to glioblastoma tumour suppression.

Masamha Chioniso P CP Xia Zheng Z Yang Jingxuan J Albrecht Todd R TR Li Min M Shyu Ann-Bin AB Li Wei W Wagner Eric J EJ

Nature 20140511 7505

The global shortening of messenger RNAs through alternative polyadenylation (APA) that occurs during enhanced cellular proliferation represents an important, yet poorly understood mechanism of regulated gene expression. The 3' untranslated region (UTR) truncation of growth-promoting mRNA transcripts that relieves intrinsic microRNA- and AU-rich-element-mediated repression has been observed to correlate with cellular transformation; however, the importance to tumorigenicity of RNA 3'-end-processi ...[more]

PMID: 24814343

Similar Datasets

CFIm25 links alternative polyadenylation to glioblastoma tumour suppression

Project description:Purpose: To identify all of the APA targets of CFIm25 on a global scale and develop an algorithm that can idenitify APA events from standard RNA-seq data Methods: RNA from HeLa cells treated with control siRNA and CFIm25 siRNA were subject to RNA-Seq. Using a custom-designed algorithm to mine RNA-seq data for novel APA events regulated by CFIm25. Results: We identified over 1,400 genes with shortened 3’UTRs after CFIm25 knockdown. Importantly, we show that as a consequence of APA, many of these mRNAs have greatly enhanced protein expression due to the loss of destabilizing features within the 3’UTR. Conclusions: Our study underscored the critical function of the CFIm complex members in governing APA and establish a previously unknown link between APA and metabolic pathways important for tumor progression.

2014-05-15 | GSE42420 | GEO

TFAM ChIP-seq in HeLa cells

Project description:ChIP-seq data characterizing the occupancy of TFAM over the mitochondrial and nuclear genomes in HeLa cells. Characterization of mitochondrial and nuclear genome-wide TFAM binding in HeLa cells

2013-09-21 | E-GEOD-48176 | biostudies-arrayexpress

Rbfox2-coordinated alternative splicing of Mef2d and Rock2 controls myoblast fusion during myogenesis

Project description:Purpose: The goals of this study are to compare transcriptomes using RNA-seq of mouse myoblasts (C2C12 cell line) in undifferentiated and differentiated states and with siRNA-mediated knock down of the RNA binding proteins, Rbfox1 (only expressed in differentiated state) and Rbfox2 (expressed in both undifferentiated and differentiated states). Methods: Differentiated and undifferentiated C2C12 cultures treated with Rbfox1 (differentiated only) or Rbfox2 siRNAs or a mock siRNA transfection were used for RNA-Seq analysis using Illumina HiSeq2000. 101x2 paired-end RNA-seq reads were first uniquely aligned to the mouse genome (mm9) using TopHat 1.4.1. RSEM was used to count the number of reads mapped to genes using UCSC database, followed by edgeR to call differentially expressed genes with false discovery rate less than 0.01. Cufflinks was used to reconstruct isoforms and analyze alternative splicing and percent spliced in (PSI) was calculated. PSI values were validated by RT-PCR. Results: 58-88% of the RNA-seq reads from technical and biological replicates mapped uniquely to the mouse genome. Analysis of gene expression and alternative splicing changes are published in Singh et al. Molecular Cell (2014). Conclusions: Our study has identified gene expression and alternative splicing transitions that occur during myoblast differentiation, demonstrate that 30% of the splicing transitions are regulated by Rbfox2, demonstrated that Rbfox2 is required for a late step of myoblast differentiation and identified two Rbfox2-regulated splicing transitions that are required for differentiation. Undifferentiated and differentiated C2C12 cultures with Rbfox2 depletion or Rbfox1 depletion (differentiated only) in at least duplicate samples analyzed by deep sequencing on Illumina HiSeq2000.

2014-07-15 | E-GEOD-58928 | biostudies-arrayexpress

Ab initio identification of transcription start sites (TSSs) in the Rhesus macaque genome by histone modification and RNA-Seq

Project description:We addressed the lack of experimentally supported transcript annotations in the Rhesus macaque genome by ab initio identification of the transcription start sites (TSSs). We took advantage of histone H3 lysine 4 trimethylation (H3K4me3)'s ability to mark TSSs and the recently developed ChIP-Seq and RNA-Seq technology to survey the transcript structures in the macaque brain. We then integrated the two types of our newly generated data with genomic sequence features and extended a TSS prediction algorithm to ab initio predict and verify 16,833 of previously electronically annotated transcription start sites at 500 bp resolution and predicted ~10,000 new TSSs. We took advantage of histone H3 lysine 4 trimethylation (H3K4me3)M-bM-^@M-^Ys ability to mark transcription start sites (TSSs) and the recently developed ChIP-Seq and RNA-Seq technology to survey the transcript structures. By integrating the ChIP-seq, RNA-seq and small RNA-seq data (previously uploaded to GEO as GSM450615 by our collaborator) with genomic sequence features and extending and improving a state-of-the-art TSS prediction algorithm, we ab initio predicted and verified previously electronically annotated TSSs at a high resolution, and predicted some novel TSSs.

2010-10-18 | E-GEOD-24538 | biostudies-arrayexpress

m6A level and isoform characterization sequencing (m6A-LAIC-seq) reveal the census and complexity of the m6A epitranscriptome

Project description:N6-methyladenosine (m6A) is a widespread reversible chemical modification of RNAs, implicated in many aspects of RNA metabolism. Little quantitative information exists as to either how many transcript copies of particular genes are m6A modified (âm6A levelsâ), or the relationship of m6A modification(s) to alternative RNA isoforms. To deconvolute the m6A epitranscriptome, we developed m6A level and isoform-characterization sequencing (m6A-LAIC-seq). We found that cells exhibit a broad range of non-stoichiometric m6A levels with cell type specificity. At the level of isoform characterization, we discovered widespread differences in use of tandem alternative polyadenylation (APA) sites by methylated and nonmethylated transcript isoforms of individual genes. Strikingly, there is a strong bias for methylated transcripts to be coupled with proximal APA sites, resulting in shortened 3â untranslated regions (3â-UTRs), while nonmethylated transcript isoforms tend to use distal APA sites. m6A-LAIC-seq yields a new perspective on transcriptome complexity and links APA usage to m6A modifications. m6A-LAIC-seq of H1-ESC and GM12878 cell lines, each cell line has two replicates

2016-06-24 | E-GEOD-66086 | biostudies-arrayexpress

Hela cell line microRNA profiles following CFIm25 knockdown

Project description:Purpose: When CFIm25 knockdown induces global APA events, we aim to investigate ceRNA landscape change based on microRNA expression change. Methods: microRNA from HeLa cells treated with control siRNA and CFIm25 siRNA were subject to RNA-Seq. Results: Consistent with our observations in TCGA breast cancer, we found a surprisingly high enrichment of 3ʹUTR shortening genes' ceRNA partners to tumor suppressors and their down-regulation. Conclusion: Our work indicated that the shortened 3ʹ-UTRs might direct the released miRNAs to repress their ceRNA partners in trans, which are enriched in ceRNET hubs and tumor suppressors, thereby effectively disrupting normal ceRNET and contributing to tumorigenesis.

2018-02-20 | GSE78198 | GEO

RNA polyadenylation landscape in human and mouse cells

Project description:Alternative polyadenylation (APA) of mRNAs has emerged as an important mechanism for post-transcriptional gene regulation in higher eukaryotes. Although microarrays have recently been used to characterize APA globally, they have a number of serious limitations that prevents comprehensive and highly quantitative analysis. To better characterize APA and its regulation, we have developed a deep sequencing-based method called Poly(A) Site Sequencing (PAS-Seq) for quantitatively profiling RNA polyadenylation at the transcriptome level. PAS-Seq not only accurately and comprehensively identifies poly(A) junctions in mRNAs and noncoding RNAs, but also provides quantitative information on the relative abundance of polyadenylated RNAs. We first analyzed HeLa cell transcriptome using PAS-Seq to demonstrate that PAS-Seq not only accurately and comprehensively identifies poly(A) junctions, but also provide quantitative information on the relativel abundance of APA isoforms. Next we analyzed the mouse embryonic stem cells, neural stem/progenitor cells, and neurons by PAS-Seq to characterize the dynamic changes of mRNA polyadenylation during stem cell differentiation.

2011-02-26 | E-GEOD-25450 | biostudies-arrayexpress

Genomewide analysis of U1C-dependent alternative splicing

Project description:To investigate whether U1C plays a role in splicing regulation in human system, we performed siRNA-mediated knockdown of U1C in HeLa cells and analyzed alternative splicing patterns by high-throughput RNA sequencing (RNAseq) RNAseq performed with poly(A)+ selected total RNA from U1C-knockdown and control-treated HeLa cells

2013-09-30 | E-GEOD-42485 | biostudies-arrayexpress

CLIP-seq of S. cerevisiae Drn1-TAP and Dbr1-TAP

Project description:Data for replicate Drn1-TAP and Dbr1-TAP CLIP-seq experiments to identify RNA-protein interactions Drn1-TAP and Dbr1-TAP CLIP-seq

2013-06-28 | E-GEOD-44959 | biostudies-arrayexpress

Compensatory induction of MYC expression by sustained CDK9 inhibition via a BRD4-dependent mechanism: Pol II occupancy profiling by ChIP-Seq in HeLa cell line in the presence or absence of CDK9 inhibition

Project description:CDK9 is the kinase subunit of P-TEFb that enables RNA polymerase (Pol) II to transit from promoter-proximal pausing to productive elongation. Although considerable interest exists in CDK9 as a therapeutic target, little progress has been made due to the lack of highly selective inhibitors. Here, we describe the development of i-CDK9 as such an inhibitor that potently suppresses CDK9 phosphorylation of substrates and causes genome-wide Pol II pausing. While most genes experience reduced expression, MYC and other primary response genes increase expression upon sustained i-CDK9 treatment. Essential for this increase, the bromodomain protein BRD4 captures P-TEFb from 7SK snRNP to deliver to target genes and also enhances CDK9’s activity and resistance to inhibition. Because the i-CDK9-induced MYC expression and binding to P-TEFb compensate for P-TEFb’s loss of activity, only the simultaneous inhibition of CDK9 and MYC can efficiently induce growth arrest and apoptosis of cancer cells, suggesting the potential of a combinatorial treatment strategy. ChIP-seq of Pol II in HeLa cells before or after i-CDk9 treatment

2015-06-17 | E-GEOD-60953 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data