Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

43 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcription profiling : Stable knockdown CUX1 knockdown in LOUCY cells lines

ABSTRACT: LOUCY cells were resuspended in Opti-MEM (Gibco) and electroporated in 4 mm cuvettes (300 V, 1000 F; Genepulser XCell, Bio-Rad) using Stealth siRNAs (Ambion) against CUX1 or negative control duplexes. Cells were rested for 15 min following electroporation before dilution into normal RPMI 10 percent FBS growth media. RNA prepared from cells 48-72 h later using an RNeasy mini kit (Qiagen) was used for cDNA preparation for microarrays according to manufacturers instructions (Illumina).

ORGANISM(S): Homo sapiens

SUBMITTER: Chi Wong

PROVIDER: E-MTAB-1833 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Gene Expression Analyisis of T-ALL LOUCY cell lines treated with ETV6 siRNA vs. scramble control siRNA

Project description:Transcriptional effects of ETV6 inactivation in immature T-ALL were investigated by gene expression analysis upon siRNA-mediated knockdown of ETV6 in LOUCY cells, a T-ALL cell line with a transcriptional program highly related to that of immature T-ALLs. Gene Set Enrichment Analysis (GSEA) of the ETV6 knockdown signature showed a significant enrichment in genes characteristically upregulated in ETV6 mutant immature T-ALLs including HOXA13, PRDM16, PTEN and CD33. 4 samples were analyzed: two biological replicates for each experimental group.

2011-11-24 | E-GEOD-33820 | biostudies-arrayexpress

H3K27ac ChIP-Seq in LOUCY

Project description:H3K27ac ChIP-Seq data of the T-ALL cell line LOUCY was obtained to find active regions in the genome and to correlate that with expression profiling of lncRNAs in the LOUCY cell line.

2016-05-17 | GSE74311 | GEO

H3K27ac ChIP-Seq in LOUCY

2016-05-17 | E-GEOD-74311 | biostudies-arrayexpress

The Histone Methyltransferases MLL1 and DOT1L Cooperate with Meningioma-1 to Induce AML [Human ChIP-seq]

Project description:Purpose: To characterize the genome-wide distribution of H3K79me2 in human leukemia cell lines treated with the Dot1l inhibitor EPZ004777 or control Methods: We performed Chip-seq for the H3K79me2 on the leukemia cell lines Mutz3, Loucy and Molm14 after 6 days in culture in the presence of 3uM EPZ004777 or DMSO control Results: H3K79me2 is completely erased from key target genes such as the HOXA cluster. Conclusions: Exposure of Mutz3, Loucy and Molm14 to 3uM EPZ004777 erases H3K79 methylation globally as well as on key loci ChIP-Seq for H3K79me2 on human leukemia cell lines exposed for 6 days to the Dot1l inhibitor EPZ004777

2016-01-12 | E-GEOD-76745 | biostudies-arrayexpress

Enzymatic methylation sequencing of LOUCY and SUP-T1 cell lines after treatment with Decitabine (3 days) or GSK3685032 (3 and 7 days)

Project description:Decitabine (DEC) has a known DNA demethylating activity but also cause cytotoxicity through DNA damage. The two differing mechanisms of action confound studies investigating the effect of DNA demethylation in cancer treatment. The novel DNA methyltransferase 1 specific inhibitor GSK-3685032 causes loss of DNA methylation without DNA damage and offers the possibility to examine the molecular consequences of global loss of DNA methylation. EM-seq was used to evaluate the DNA demethylating effects of DEC and GSK-3685032 in LOUCY and SUP-T1 cells treated with 10 nM Decitabine for 3 days or 300 nM of GSK-3685032 for 3 and 7 days.

2024-10-13 | E-MTAB-14202 | biostudies-arrayexpress

Effect of 48h treatment with 100nM GSK2879552 on T-ALL cell lines LOUCY and PEER

Project description:RNA sequencing was performed on biological triplicates of LOUCY and PEER cells treated with 100nM GSK2879552 for 48h versus their corresponding DMSO treatment controls. GSK2879552 is a potent, selective and orally bioavailable inhibitor of the lysine-specific histone demethylase 1 (LSD1). Gene expression was severely affected by LSD1 inhibition. Pathway analysis performed on the differentially expressed genes following 48hrs of LSD1i treatment clearly showed an increased apoptotic gene signature (CASP3, CASP8) and enhanced expression of genes associated with TRAIL signaling. Furthermore, pre-ranked Gene Set Enrichment Analysis (GSEA) revealed that genes upregulated after LSD1 inhibition in LOUCY showed significant enrichment for transcripts that are down in hematopoietic stem cells and early T lymphocytes. In contrast, important components of the Notch, WNT and SMAD signalling complex were significantly down regulated upon short-term LSD1i treatment in LOUCY cells. In line with this notion, pre-ranked GSEA also revealed that LSD1i resulted in decreased expression of genes that significantly overlap with an oncogenic MYC signature.

2017-02-03 | GSE83126 | GEO

Gene expression signature of the T-ALL cell line LOUCY treated with 250nM (+)-JQ1 for 4h

Project description:We analyzed the transcriptional consequences of the BET bromodomain inhibitor JQ1 in the T-ALL cell line LOUCY by microarray analysis. Short-term exposure to a low dose of JQ1 (4h, 250nM) provided insights in the genes whose expression was immediately affected by BET bromodomain inhibition. Significantly downregulated genes upon short-term drug treatment included stem-cell associated genes and putative oncogenes such as BAALC, WT1, MN1, MEF2C, LMO1 and LMO2. Genes associated with the 500 highest ranked enhancer regions in LOUCY, were significantly enriched in genes downregulated after JQ1 treatment.

2016-12-15 | GSE81915 | GEO

Next generation sequencing following CUX1 knockdown in erythroblasts

Project description:Anemia is a significant cause of morbidity and mortality in myeloid malignances. Cytogenetic changes are recurrent within malignant hematopoietic stem and progenitor cells, yet their role in anemia pathogenesis remains unknown. One recurrent karyotypic abnormality in myeloid neoplasms is the deletion of part or all of chromosome 7 [-7/del(7q)], which harbors the transcription factor and tumor suppressor gene, CUX1. CUX1 knockdown mouse models develop myeloid disease similar to that seen in humans, including a spontaneous, cell intrinsic, and lethal anemia that develops with age. Here, we elucidate the cellular and molecular mechanisms by which CUX1 regulates erythropoiesis. We demonstrate CUX1 knockdown mice have an aberrant stress erythropoiesis response and decreased survival after acute anemia induction. CUX1 insufficient erythroblasts undergo accelerated cell cycling and increased apoptosis. In line with these phenotypes, transcriptome profiling indicates that CUX1-knockdown elicits increased proliferation and decreased erythroid differentiation gene signatures. ATAC-sequencing demonstrated dramatic, global chromatin opening in CUX1-knockdown erythroblasts. As measured by fluorescence lifetime imaging, this increased chromatin accessibility is concomitant with a disruption in nuclear condensation, which is normally requisite in mammalian erythroblasts for nuclear eviction and terminal differentiation. Finally, we show that CUX1 mediates chromatin compaction by promoting histone deacetylation. Thus, rather than a transcriptional role, our data implicate in an epigenetic regulatory role for CUX1 in erythropoiesis. Furthermore, these results suggest therapeutic targeting of epigenetic regulators, such as histone acetyl transferases, may have clinical benefit for the anemias associated with loss of CUX1.

2021-08-10 | GSE181626 | GEO

Low pass whole methylome enzymatic sequencing of 11 T-ALL cell lines untreated and after treatment with different concentrations of 5-azacytidine (AZA), 5-aza-2′-deoxycytidine (DEC) and GSK3685032 (GSK5032) for 3 and 7 days

Project description:Here we performed low coverage whole genome enzymatic-mehtyl-conversion sequencing (EM-seq) of 11 commercially available T-ALL cell lines to evaluate their global DNA methylation profile. We then proceeded to treat ALL-SIL, SUP-T1, LOUCY and JURKAT with varying concentrations (0-3000 nM) of three different hypomethylating agents, 5-azacytidine (AZA), 5-aza-2′-deoxycytidine (DEC) and GSK3685032 (GSK5032), for 3 and 7 days to evaluate their DNA demethylating ability.

2024-10-13 | E-MTAB-14197 | biostudies-arrayexpress

Gene Expression Analyisis of T-ALL LOUCY cell lines treated with ETV6 siRNA vs. scramble control siRNA

2011-11-24 | GSE33820 | GEO