Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

12 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcription profiling of human U266, MM.1s, KMS11, 8226/S multiple myeloma cell lines treated with arsenic

ABSTRACT: We used microarrays to examine changes in gene expression in multiple myeloma cell lines following treatment with arsenic trioxide and darinaparsin Experiment Overall Design: Four multiple myeloma cell lines (U266, MM.1s, KMS11, 8226/S) were treated with either arsenic trioxide (ATO) for 6, 24, or 48 hours or darinaparsin (DAR) for 6 or 24 hours; RNA was extracted from treated and control cells for microarray analysis

ORGANISM(S): Homo sapiens

SUBMITTER: Larry Boise

PROVIDER: E-GEOD-14519 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Publications

Darinaparsin induces a unique cellular response and is active in an arsenic trioxide-resistant myeloma cell line.

Matulis Shannon M SM Morales Alejo A AA Yehiayan Lucy L Croutch Claire C Gutman Delia D Cai Yong Y Lee Kelvin P KP Boise Lawrence H LH

Molecular cancer therapeutics 20090505 5

Here, we report on the organic arsenical darinaparsin (ZIO-101, S-dimethylarsino-glutathione) and its anti-myeloma activity compared with inorganic arsenic trioxide. Darinaparsin induced apoptosis in multiple myeloma cell lines in a dose-dependent manner, and the addition of N-acetylcysteine, which increases intracellular glutathione (GSH), blocked cytotoxicity of both darinaparsin and arsenic trioxide. In contrast to arsenic trioxide, intracellular GSH does not appear to be important for darina ...[more]

PMID: 19417148

Similar Datasets

human leukemia cell line K562 offspring acquring imatinib resistance(K562-r) : Control vs. Drug treated

Project description:Transcriptional profiling of K562-r comparing control untreated human leukemia cells with human leukemia cells treated with AMN107 and ATO individually or combined.Four timepoints included are 3h,12h,24h,48h, covering the whole time window of K562-r cells responsing to the drug treatment.At the combination of 1.5uM ATO and 8uM AMN107, K562-r cells have the most significant coordinated effects (the apoptosis rate at 72h was 56.41% compared to 12.23% in ATO alone and 29.8% in AMN107 alone.). We studied gene expression series in K562-r cells with or without drug treatments by cDNA microarray analysis. Many genes involved in endoplasmic reticulum (ER) stress signaling, including ATF3, DDIT3, HERPUD1, HSPA5, XBP1 and TXNDC12, were highly up-regulated within 12 h of co-treatment, suggesting that the combination of ATO with AMN107 induced an ER stress response leading to apoptosis later on. Other ER-stress markers like the JNK pathway, which bridges the ER-stress and apoptosis, have been activated. Knock down the initiator of JNK partially alleviate the effects of apoptosis (p<0.05). Co-administering AMN107 and arsenic trioxide, inducing apoptosis via the ER-stress, indicates a novel therapy alternative for the imatinib induced secondary resistance. 17-condition experiment, untreated K562-r vs. Drug-treated K562-r cells, including 4 time points, for each point the untreated and 1.5uM ATO treated,8uM AMN107 treated and both 1.5uM ATO and 8uM AMN107 treated, independently grown and harvested. One replicate per array. Untreated K562-r_0h used to counteracting the background.

2010-12-30 | E-GEOD-24946 | biostudies-arrayexpress

Arsenic targets Pin1 and cooperates with retinoic acid to inhibit cancer-driving pathways and tumor-initiating cells

Project description:Arsenic trioxide (ATO) and all-trans retinoic acid (ATRA) combination safely cures fatal acute promyelocytic leukemia, but the mechanisms underlying their action and synergy remain elusive. ATRA inhibits APL, breast and liver cancers by targeting isomerase Pin1, a master regulator of oncogenic signaling. Here we show that ATO targets Pin1 and cooperates with ATRA to exert potent anticancer activity. ATO inhibits and degrades Pin1, and suppresses its oncogenic function by noncovalent binding to Pin1’s active site. ATRA increases cellular ATO uptake through upregulating aquaporin-9. ATO and ATRA, at clinically safe doses, cooperatively ablate Pin1 to block numerous cancer-driving pathways and inhibit the growth of triple-negative breast cancer cells and tumor-initiating cells in cell and animal models including patient-derived orthotopic xenografts, similar to Pin1 CRISPR knockout, which is substantiated by comprehensive protein and microRNA analyses. Thus, synergistic Pin1 inhibition by ATO and ATRA offers an attractive approach to combating breast and other cancers.

2018-10-16 | PXD010224 | Pride

Comparison of gene expression profile of naive versus arsenic trioxide resistant acute promyelocytic leukemia cell line NB4

Project description:The aim of this study was to gain insight into the potential mechanism of resistance to arsenic trioxide (ATO). The gene expression profile of naive (NB4) (Acute promyelocytic leukemia (APL) cell line and one of its in house generated ATO resistant sub clone (NB4-VM-AsR1) was done using whole genome microarray and compared to generate the differential expression profile which will give insight into the mechanisms of ATO resistance in APL. Agilent one-color experiment,Organism: Human ,Agilent Whole Genome Human 4x44k (AMADID: 014850) , Labeling kit: Agilent Quick-Amp labeling Kit (p/n5190-0442) naive versus arsenic trioxide resistant acute promyelocytic leukemia cell line NB4

2013-08-02 | E-GEOD-42031 | biostudies-arrayexpress

The genomic landscape of sensitivity to Arsenic Trioxide characterized by Genome-wide CRISPR-Cas9 screening

Project description:The key modifiers of sensitivity to Arsenic Trioxide (ATO) remained unclear, and we presented a genome-wide scale loss-of-function screening to identify the modulators of cell response to ATO.

2023-04-24 | GSE218982 | GEO

ATO treatment on mesenchymal stem cells (MSCs) interacting breast cancer cells

Project description:Based on next generation RNA-seq, we examed Arsenic trioxide treatment (ATO) effect on MSCs-interacting MCF7 cells in 3D cultures. We found gap junction protein Cx43 is dramatically downregulated after ATO treatment..

2018-10-01 | GSE118923 | GEO

Comparing Gene Expression Profiling of ATO sensitive and Resistant cell lines

Project description:To further characerize the arsenic trioxide (ATO) resistance in acutepromyelocytic leukemia, we had made NB4 cell line (arsenic sensitive) to be resistant to arsenic by exposing them to increasing concentration till they are resistant to it and we named it NB4-EV-AsR1. We have also used another cell line (UF1) which is by default resistant to arsenic. Comparing the GEP will give us novel pathways that can contirbute to arseic trioxide.

2019-06-01 | GSE115812 | GEO

Gene expression from total and polysomal RNA fractions after ATO treatment in LN229 cells.

Project description:Arsenic trioxide (ATO) treatment leads to activation of mRNA translation through the MAPK-interacting kinase (MNK) signaling pathway. Polysomal fractionation and microarray analysis allows for identification of transcripts undergoing active translation. We identified the genes differentially enriched in untreated and ATO treated fractions. In this dataset, we include expression data in untreated and ATO treated LN229 cells using either the total or polysomal RNA.

2018-01-01 | GSE100523 | GEO

Transcription profiling of two human myeloma cells lines incubated with and without leptin

Project description:The effect of recombinant leptin (100 ng/ml) on gene expression in two human myeloma cell lines (RPMI 8226 and ANBL-6) were studied in cells incubated with and without leptin for 24 h.

2006-11-27 | E-MEXP-921 | biostudies-arrayexpress

Arsenic trioxide inhibits lung metastasis of breast cancer by suppression of TP53, TGFβ and TNFα signaling pathways

Project description:Metastasis is the main cause of mortality of breast cancer. To explore the mechanisms of arsenic trioxide (ATO) in inhibition of breast cancer metastasis, ATO regulated genes in breast cancer MDA-MB-231 and LM2-4175 cells were studied. After data analysis, ATO regulated genes were involved in TP53, TGFβ and TNFα signaling pathways. Furthermore, TGFβ and TNFα activated genes in breast cancer MDA-MB-231 cells were studied.

2023-04-16 | GSE184828 | GEO

Comparison of gene expression profile of naive versus arsenic trioxide resistant acute promyelocytic leukemia cell line NB4

2013-08-02 | GSE42031 | 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