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K562 Gene Expression Control vs 1R-Chl treatments

ABSTRACT: To determine whether the polyamide-Chl conjugate 1R-Chl would cause similar changes in global gene expression in K562 cells, affymetrix gene chip analysis was performed using 1R-Chl. Through class comparison analysis, 1R-Chl affected the levels of transcription and genes of interest were determined. Keywords: Treatment response

ORGANISM(S): Homo sapiens

PROVIDER: GSE8832 | GEO | 2007/08/22

SECONDARY ACCESSION(S): PRJNA102165

REPOSITORIES: GEO

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Transcription profiling of the human K562 cell line treated with the polyamide-Chl conjugate 1R-Chl

Project description:To determine whether the polyamide-Chl conjugate 1R-Chl would cause similar changes in global gene expression in K562 cells, affymetrix gene chip analysis was performed using 1R-Chl. Through class comparison analysis, 1R-Chl affected the levels of transcription and genes of interest were determined. Experiment Overall Design: K562 cells were incubated with 1R-Chl (at 250 nM) or in the absence of polyamide, in triplicate for 24 h before RNA purification and microarray analysis at The Scripps Research Institute microarray facility. Affymetrix U133A Plus 2.0 GeneChips were hybridized in groups of three for each of the two groups. The Affymetrix probe set data were imported into BRB Arraytools (3.5.0 Beta 2), selecting the U133 chips used in the experiment and leaving all filters off.

2008-06-16 | E-GEOD-8832 | biostudies-arrayexpress

Homo sapiens

Project description:K562 Gene Expression Control vs 1R-Chl treatments

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Project description:Transcription profiling by array of human K562 cells treated with 1R-Chl

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Expression data of cHL cell lines after FOXO1 activation

Project description:FOXO1 is highly expressed in normal B cells and in most types of non-Hodgkinl lymphoma. In Hodgkin and Reed-Sternberg cells of classical Hodgkin lymphoma(cHL) expression of FOXO1 is low or absent. We overexpressed constitutively active mutant of FOXO1 fused in frame with estrogen receptor ligand-binding domain (FOXO1(3A)ER), which can be activated by 4-Hydroxytamoxifen (4-OHT), in cHL cell lines KM-H2 and L428. Activation of the FOXO1 with 4-OHT resulted in inhibition of proliferation and apoptosis. Using gene-expression array we found that FOXO1 activates transcription of known and potential tumor suppressor genes: CDKN1B, PMAIP1, BCL2L11, TNFSF10, FBXO32, CBLB). Of note, FOXO1 repressed transcription of several cytokines and cytokine receptors, which are known tobe involved in pathogenesis of cHL (e.g. CCL5, CXCR5, TNFRSF8). Taken togather our data indicate important role of FOXO1 repression in pathogenesis of cHL.

2012-06-01 | GSE29545 | GEO

Ribosomal profiling of CRISPR edited and parental CHL-1 cell line

Project description:Ribosomal stress was evaluated in melanoma cell line CHL-1 after CRISPR editing genomic locus containing SNORD50A/B We have used CRISPR genome editing tool to KD snoRNAs SNORD50A/B from CHL-1 genome and assessed ribosomal binding genome-wide using ribosome profiling

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Immune and stromal transcriptional patterns in cHL

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Expression data of cHL cell lines after KLF4 activation

Project description:Characteristic extinguishing of B-cell phenotype in cHL is believed to be a result of transcription factor network deregulation due to the overexpression of repressor proteins ID2 and ABF-1. KLF4 is a versatile transcription factor, participating in regulation of differentiation processes in various tissues. Epigenetic silencing of KLF4 in cHL hints that KLF4 is involved in the complex mechanism of extinguishing of B-cell phenotype in cHL. To clarify this issue we investigated transcriptome changes, induced by KLF4 activation in two cHL cell lines KM-H2 and L428. KM-H2-KLF-ER and L428-KLF-ER cells were incubated with 200 ÂµM 4-OHT or vehicle (ethanol). The experiment was done twice. After 24 h, total RNA was isolated with RNeasy mini kit (QIAGEN). Microarray analyses were performed using 200 ng total RNA as starting material and 5.5 Âµg ssDNA per hybridization (GeneChip Fluidics Station 450; Affymetrix, Santa Clara, CA). The total RNAs were amplified and labeled following the Whole Transcript (WT) Sense Target Labeling Assay (http://www.affymetrix.com). Labeled ssDNA was hybridized to Human Gene 1.0 ST Affymetrix GeneChip arrays (Affymetrix, Santa Clara, CA). The chips were scanned with a Affymetrix GeneChip Scanner 3000 and subsequent images analyzed using AffymetrixÂ® Expression Console Software (Affymetrix). Probe level data were obtained using the robust multichip average (RMA) normalization algorithm.

2010-10-22 | E-GEOD-21296 | biostudies-arrayexpress

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