Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

TsRNA microarray of parental normal-like and breast cancer cell lines and with inhibited or induced RUNX1 expression

ABSTRACT: tsRNA microarray of parental normal-like and breast cancer cell lines and with inhibited or induced RUNX1 expression

PROVIDER: PRJNA596783 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

tsRNA microarray of parental normal-like and breast cancer cell lines and with inhibited or induced RUNX1 expression

Project description:The expression levels of tRNA-derived small RNA, known as tsRNA, were interrogated in the following parental cell lines: MCF10A normal-like mammary epithelial cell, MCF7, MCF10AT1, MCF10CA1a, and MDA-MB-231 breast cancer cells. In addition, tsRNA expression was determined after shRNA-inhibition of RUNX1 in MCF10A cells or RUNX1 induction in MCF10CA1a cells.

2020-01-01 | GSE142382 | GEO

Genomic binding of RUNX1 in MCF10A cells

Project description:The overall goal of this study is to identify the genomic binding of RUNX1 in MCF10A cells. We used ChIPseq (chromatin immunoprecipitation assay followed by deep sequencing) to identify the binding sites of RUNX1 in MCF10A cells. We performed ChIPseq of RUNX1 using parental MCF10A cells and did not identify high confident binding sites. To overcome this hurdle, we first generated a RUNX1 deleted MCF10A cell line using CRISPR-Cas9. We then transduced this RUNX1 KO MCF10A cells with lentiviruses that inducibly expresses RUNX1. After treating RUNX1 inducible MCF10A cells with 1 ug/ml doxycycline for 24 hours, we performed ChIPseq of RUNX1.

2019-04-18 | GSE129314 | GEO

ChIP-seq for RUNX1 and ETV6-RUNX1 in B-ALL cell lines and patient samples

Project description:Identification of RUNX1 and ETV6-RUNX1 binding sites

2022-04-10 | E-MTAB-10312 | biostudies-arrayexpress

Microarray gene expression analyses of HCT116 parental and isogenic p53KO cell lines

Project description:Untreated cells were used for analysis of the basal gene expression levels in HCT116 parental and isogenic p53KO cell lines grown to confluency to elucidate the genes/pathways that are differentially regulated and dependent on the p53 pathway.

2023-01-02 | GSE207647 | GEO

Differential response to Lenalidomide from WT and RUNX1-KO MDS-L del(5q) cells

Project description:We used CRISPR/Cas9 system to generate WT Control and RUNX1-KO MDS-L cells isolated as single clones from the parental MDS-L cell line. We have observed that RUNX1-KO MDS-L cells are resistant to Lenalidomide-induced cell death compared to WT Control MDS-L cells We have treated WT and RUNX1-KO MDS-L cells with 1µM Lenalidomide for 24h or 72h and performed expression analysis

2020-01-28 | GSE126265 | GEO

RUNX1 isoforms in leukemogenesis

Project description:Aneuploidy and structural aberrations affecting chromosome 21 (Hsa21) are the most frequent in cytogentic events in acute myeloid leukemia. However, it remains unclear why leukemic blasts select for amplifications of Hsa21 or parts of it and why children with Down syndrome (i.e. trisomy 21) are at a high risk of developing leukemia. Here, we propose that disequilibrium of the RUNX1 isoforms and resultant RUNX1A dominance are key to trisomy 21-associated leukemogenesis. Using a Hsa21-focussed CRISPR-Cas9 screen, we uncovered a strong and specific RUNX1 dependency in myeloid leukemia associated with Down syndrome (ML-DS). High levels of RUNX1A – as seen in ML-DS – synergized with the pathognomonic Gata1s mutation in ML-DS pathogenesis, an effect that was reversed upon restoration of the normal RUNX1A:RUNX1C equilibrium. Mechanistically, RUNX1A displaces RUNX1C from its endogenous binding sites and recruits the MYC cofactor MAX to induce oncogenic programs and perturb normal differentiation. This presents a therapeutic vulnerability that can be exploited by interfering with MYC:MAX dimerization. Our study highlights the importance of alternative splicing in leukemogenesis, and paves the way for developing specific and targeted therapies for ML-DS as well as for other leukemias with Hsa21 aneuploidy or RUNX1 isoform disequilibrium.

2023-05-10 | PXD030616 | Pride

HDAC3 preferentially binds to RUNX1 in t(8;21) AML cells and collaborates with RUNX1 to repress AML1-ETO-mediated transcriptional activation

Project description:Human histone deacetylase 3 (HDAC3) plays an important role in gene transcription in diseased human cells, such as leukemia. The t(8;21) chromosomal translocation is one of the most commonly observed genetic abnormalities associated with acute myeloid leukemia. This translocation generates the AML1-ETO fusion protein between the wild-type RUNX1 transcription factor and wild-type ETO transcriptional corepressor. To better understand the role of HDAC3 in t(8;21) leukemogenesis, the human HDAC3-containing complexes were isolated from stably-transfected HeLa cells by using anti-FLAG immunoprecipitation. The resulting complexes were resolved in SDS-PAGE. The components of the complexes were identified using LC-MS/MS. We report here that the human RUNX1 transcription is a component of the HDAC3 complexes. We demonstrate that HDAC3 and RUNX1 collaboratively repress AML1-ETO-mediated transcription. These results reveal new insight into how AML1-ETO, RUNX1, and HDAC3 crosstalk to deregulate gene transcription in t(8;21) leukemia cells.

2020-02-17 | PXD017230 | Pride

Transcription profiling of human normal progenitor cells mutated for RUNX1-RUNX1 during myeloid and erythroid development to identify genes disregulated by RUNX1-RUNX1

Project description:In order to identify genes dysregulated by the aberrant transcriptional activity of RUNX1-RUNX1T1, we used microarrays to determine the effect of this mutation on gene expression during myeloid and erythroid development of normal human progenitor cells.

2007-10-01 | E-MEXP-583 | biostudies-arrayexpress

ChIP-seq for RUNX1 and ETV6-RUNX1 in an induced pluripotent stem cell model of ETV6-RUNX1 pre-leukaemia

Project description:ETV6-RUNX1 is a first-hit mutation in childhood B cell precursor acute lymphoblastic leukaemia. ETV6-RUNX1 is a fusion protein which inherits the DNA-binding runt domain from RUNX1. Here we performed chromatin precipitation for native RUNX1 and ETV6-RUNX1 using RUNX1 antibodies and specifically for the ETV6-RUNX1 fusion using a V5-tag pull down.

2022-10-31 | E-MTAB-12208 | biostudies-arrayexpress

RNA-sequencing data analysis of PC9 cell lines

Project description:The function of tsRNA-5001a on the growth of tumor cells was studied by cell function experiment. RT-qPCR was used to detect the expression of tsRNA-5001a in paired samples of lung adenocarcinoma. Cell localization of tsRNA-5001a was performed by nuclear-cytoplasmic separation assay. Transcriptome sequencing was used to screen the molecules involved in the regulatory network of tsRNA-5001a.

2021-12-14 | GSE179341 | 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