Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

8 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

KSHV-vGPCR induces genomic instability in a miR-34a-dependent manner

ABSTRACT: Cell lines of a vGPCR-driven tumor model have been compared to identify KSHV-vGPCR-dependent mechanisms of tumor progression. Cell lines include two biological replicates of a vGPCR-transformed tumor cell line (vGPCR-TC#1+#2) generated by passaging a vGPCR-BALB/c-3T3 cell line (also included) through athymic nude and BALB/c mice. A vGPCR-knockdown tumor cell line (derived from vGPCR-TC#1 generated by lentiviral knockdown) and a GFP-transduced control BALB/c-3T3 cell line are included as well. Data also include a vGPCR-TC#1-derived cell line were miR-34a-5p was knocked down using a Tough Decoy RNA, called TuDmiR-34a-TC#1. Additionally, two miR-34a overexpressing cell lines have been generated derived from the parental vGPCR-3T3 cells and the tumor cell line vGPCR-TC#2 named miR-34a-vGPCR-3T3 respectively miR-34a-vGPCR-TC#2.

ORGANISM(S): Mus musculus

SUBMITTER: Claudia Krause

PROVIDER: E-MTAB-3393 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Identification of SART3 as a pre-miR-34a–binding protein

Project description:MicroRNAs (miRNAs or miRs) are small, noncoding RNAs that are implicated in the regulation of nearly all biological processes. Global miRNA biogenesis is altered in many cancers and RNA-binding proteins (RBPs) have been shown to play a role in this process, presenting a promising avenue for targeting miRNA dysregulation in disease. miR-34a exhibits tumor-suppressive functions by targeting cell cycle regulators CDK4/6 and anti-apoptotic factor Bcl-2, among other regulatory pathways such as Wnt, TGF-, and Notch signaling. Many cancers show downregulation or loss of miR-34a, and synthetic miR-34a supplementation has been shown to inhibit tumor growth in vivo; however, the post-transcriptional mechanisms by which miR-34a is lost in cancer are not entirely understood. Here, we have used a proteomics-mediated approach to identify Squamous cell carcinoma antigen recognized by T-cells 3 (SART3) as a putative pre-miR-34a-binding protein. SART3 is a spliceosome recycling factor and nuclear RBP with no previously reported role in miRNA regulation. We demonstrate that SART3 binds pre-miR-34a with specificity over pre-let-7d and begin to elucidate a new functional role for this protein in non-small lung cancer cells. Overexpression of SART3 led to increased miR-34a levels, downregulation of the miR-34a target genes CDK4 and CDK6, and cell cycle arrest in the G1 phase. In vitro binding studies showed that the RNA-recognition motifs within the SART3 sequence are responsible for selective pre-miR-34a binding. Collectively, our results present evidence for an influential role of SART3 in miR-34a biogenesis and cell cycle progression.

2019-10-14 | PXD015278 | Pride

miR-34a and miR-34b/c suppress intestinal tumorigenesis in ApcMin/+ Mice

Project description:miR-34a and miR-34b/c genes are frequently epigenetically silenced in primary CRCs. However, the in vivo relevance of miR-34a/b/c for suppression of intestinal tumor formation has not been analyzed by genetic approaches. ApcMin/+ mice with deletion of the miR-34a and miR-34b/c genes were generated and analyzed. The mRNA expression profiles of intestinal adenomas with and without functional miR-34a/b/c genes were compared.

2017-05-28 | GSE84138 | GEO

CSF1R mediates effects of miR-34a loss during intestinal tumorigenesis in ApcMin mice (tumor organoid)

Project description:To address the in vivo relevance of CSF1R regulation by miR-34a during intestinal tumor formation, we generated ApcMin/+ mice with intestinal-epithelial cell (IEC)-specific deletions of the Mir34a and/or Csf1r genes. The mRNA expression profiles of tumor organoids derived ffrom intestinal adenomas with and without functional miR-34a and/or Csf1r were compared.

2022-10-04 | GSE167449 | GEO

CSF1R mediates effects of miR-34a loss during intestinal tumorigenesis in ApcMin mice (adenoma)

Project description:To address the in vivo relevance of CSF1R regulation by miR-34a during intestinal tumor formation, we generated ApcMin/+ mice with intestinal-epithelial cell (IEC)-specific deletions of the Mir34a and/or Csf1r genes. The mRNA expression profiles of intestinal adenomas with and without functional miR-34a and/or Csf1r were compared.

2022-10-04 | GSE167448 | GEO

Identification of copy number changes in cell lines of a vGPCR-driven mouse tumor model

Project description:Genomic DNA of KSHV-vGPCR-transformed tumor cell lines (vGPCR-BTC#1+#2), vGPCR-transformed 3T3 cell lines and a GFP-3T3 control cell line was cohybridized with normal BALB/c reference genomic DNA. gDNA of cell lines labeled with Cy3 gDNA of reference DNA labeled with Cy5

2016-02-09 | E-MTAB-3394 | biostudies-arrayexpress

p53-regulated networks of protein, mRNA, miRNA and lncRNA expression revealed by integrated pSILAC and NGS analyses

Project description:We determined the effect of p53 activation on de novo protein synthesis using quantitative proteomics of newly synthesized proteins (pulsed stable isotope labeling with amino acids in cell culture, pSILAC) in combination with mRNA and non-coding RNA expression analyses by next generation sequencing (RNA-, miR-Seq) in the colorectal cancer (CRC) cell line SW480. Furthermore, genome-wide DNA binding of p53 was analyzed by chromatin-immunoprecipitation (ChIP-Seq). Thereby, we identified differentially regulated mRNAs (1258 up, 415 down), miRNAs (111 up, 95 down), lncRNAs (270 up, 123 down) and proteins (542 up, 569 down). Changes in mRNA and protein expression levels showed a positive correlation (r = 0.50, p < 0.0001). More transcriptionally induced genes displayed occupied p53 binding sites (4.3% mRNAs, 7.2% miRNAs, 6.3% lncRNAs, 5.9% proteins) than repressed genes (2.4% mRNAs, 3.2% miRNAs, 0.8% lncRNAs, 1.9% proteins), suggesting indirect mechanisms of repression. Around 50% of the downregulated proteins displayed seed-matching sequences of p53-induced miRNAs in the corresponding 3’-UTRs. Moreover, proteins repressed by p53 significantly overlapped with those previously shown to be repressed by miR-34a. We confirmed upregulation of the novel direct p53 target genes LINC01021, MDFI, ST14 and miR-486 and showed that ectopic LINC01021 expression inhibited proliferation in SW480 cells. Furthermore, HMGB1, KLF12 and CIT mRNAs were confirmed as direct targets of the p53-induced miR-34a, miR-205 and miR-486-5p, respectively. In line with the loss of p53 function during tumor progression, elevated expression of HMGB1, KLF12 and CIT was detected in advanced stages of cancer. This study provides new insights and a comprehensive catalogue of p53-mediated regulations and p53 DNA binding in CRC cells.

2015-07-23 | PXD001976 | Pride

Profiling of microRNA expression in lung cancer cells with up-regulation of Zeb1

Project description:The Zeb1 transcriptional repressor plays a key role in metastasis through the down-regulation of genes that are strong inducers of epithelial differentiation and inhibitors of stem-ness. Here we report that Zeb1 controls the expression of numerous oncogenic and tumor suppressive microRNAs (miRs). Zeb1 stimulated pro-migratory cytoskeletal processes by down-regulating miR-34a and activated Rho GTPases through Arhgap1, a Cdc42 GTPase activating protein and novel miR-34a target gene. Poor-prognosis human lung adenocarcinomas were highly enriched in a cytoskeletal gene signature activated by miR-34a down-regulation. These findings suggest that Zeb1 regulates a miR network and drives pro-migratory cytoskeletal processes through miR-34a. Microarray-based interrogation of global miR expression changes in a non-metastatic KP cell line (393P) that undergoes EMT and gains invasive and metastatic capabilities following forced Zeb1 expression (393P_Zeb1). two group comparison

2012-08-08 | E-GEOD-38386 | biostudies-arrayexpress

Poll II ChIP-Seq in miR-34a transfectant

Project description:To investigate the behavior of RNA Pol II during RNA activation by miR-34a,the ChIP-Seq analysis of RNA Poll II in NCI-H1299 cell line was performed. This experiment analyzes how RNA pol II is activated by the introduction of miR-34a in some genes whose transcription is induced by miR-34a. From the analysis of this data, the purpose is to clarify the molecular mechanism of RNA activation by miR-34a.

2021-02-01 | GSE161321 | GEO

Gene and microRNA expression profiling of a melanoma cell line resistant to BRAF inhibitor PLX4032 compared to the parental sensitive counterpart (mRNA)

Project description:Gene and microRNA expression profiles were generated for a melanoma cell line resistant to the BRAF inhibitor PLX4032 and its parental cell line in order to identify altered gene-microRNA regulatory networks. Results showed that CCL2 acts as an autocrine factor and coordinately regulates, via HIF1, miR-34a, miR-100 and miR-125b, which are involved in cell proliferation and apoptosis. Inhibition of CCL2 and of the specific miRNAs restores sensitivity to BRAF inhibitors.

2016-02-01 | GSE68840 | GEO

Gene and microRNA expression profiling of a melanoma cell line resistant to BRAF inhibitor PLX4032 compared to the parental sensitive counterpart (miRNA)

2016-02-01 | GSE68839 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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