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Expression data from MDA-MB-231 cells treated with vehicle or YW3-56

ABSTRACT: PAD4 is overexpressed in many cancer cells. We developed PAD inhibitors that efficiently inhibit the cancer cell growth. One inhibitor YW3-56 could efficiently induce cell death of triple negative breast cancer MDA-MB-231 cells. We used microarray to detail the global gene expression of MDA-MB-231 before and after YW3-56 treatment and identify significant up-regulated or down-regulated genes by YW3-56 MDA-MB-231 cells were cultured and treated with vehicle (DMSO) or YW3-56. Cells were washed with PBS and harvested for RNA extraction and hybridization on Affymetrix microarray.

ORGANISM(S): Homo sapiens

SUBMITTER: Yanming Wang

PROVIDER: E-GEOD-46590 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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ATF4 Gene Network Mediates Cellular Response to the Anticancer PAD Inhibitor YW3-56 in Triple-Negative Breast Cancer Cells.

Wang Shu S Chen Xiangyun Amy XA Hu Jing J Jiang Jian-Kang JK Li Yunfei Y Chan-Salis Ka Yim KY Gu Ying Y Chen Gong G Thomas Craig C Pugh B Franklin BF Wang Yanming Y

Molecular cancer therapeutics 20150122 4

We previously reported that a pan-PAD inhibitor, YW3-56, activates p53 target genes to inhibit cancer growth. However, the p53-independent anticancer activity and molecular mechanisms of YW3-56 remain largely elusive. Here, gene expression analyses found that ATF4 target genes involved in endoplasmic reticulum (ER) stress response were activated by YW3-56. Depletion of ATF4 greatly attenuated YW3-56-mediated activation of the mTORC1 regulatory genes SESN2 and DDIT4. Using the ChIP-exo method, hi ...[more]

PMID: 25612620

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Expression data from MDA-MB-231 cells treated with vehicle or YW3-56

Project description:PAD4 is overexpressed in many cancer cells. We developed PAD inhibitors that efficiently inhibit the cancer cell growth. One inhibitor YW3-56 could efficently induce cell death of triple negative breast cancer MDA-MB-231 cells. We used microarray to detail the global gene expression of MDA-MB-231 before and after YW3-56 treatment and identify significant up-regulated or down-regulated genes by YW3-56

2015-05-21 | GSE46590 | GEO

Tang2019 - Pharmacology modelling of AURKB and ZAK interaction in TNBC

Project description:Aurora Kinase B and ZAK interaction model Equivalent of the stochastic model used in "Network pharmacology model predicts combined Aurora B and ZAK inhibition in MDA-MB-231 breast cancer cells" by Tang et. al. 2018. The only difference is cell division and partitioning of the components, which are available in the original model for SGNS2.

2024-09-02 | BIOMD0000000940 | BioModels

MDA-MB-231 Breast Cancer Bone Tropic vs Parental Hypoxic Secretome Analysis

Project description:The project profiled the expression patterns in hypoxia induced secretomes between MDA-MB-231 parental and MDA-MB-231 Bone Tropic (BT) breast cancer cell lines which have been previously generated by Massague and colleagues (Kang et al. Cancer Cell 2003).

2017-03-29 | MSV000080797 | MassIVE

Expression data from active human umbilical cord mesenchymal stem cell (active HUMSC) and inactive human umbilical cord mesenchymal stem cell (inactive HUMSC)

Project description:Active HUMSC with distinct binding rate to MDA MB-231 breast cancer cells, distinct ability in suppressing tumorigenesis,distinct cell in cell features and distinct features under TEM then inactive HUMSC We used microarrays to detail the difference gene expression between active HUMSC and inactive HUMSC HUMSC with high MDA MB-231 breast cancer cells suppression rate was selective as active HUMSC and HUMSC with low MDA MB-231 breast cancer cells suppression rate was selective as inactive HUMSC

2012-12-31 | E-GEOD-27820 | biostudies-arrayexpress

Expression data from MDA-MB-231 parental and xenograft tumor cells treated with Smac mimetic SM-164.

Project description:Small-molecule Smac mimetics target inhibitor of apoptosis (IAP) proteins to induce TNFÎ±-dependent apoptosis in cancer cells and several Smac mimetics have been advanced into clinical development as a new class of anticancer drugs. However, preclinical studies have shown that only a small subset of cancer cell lines are sensitive to Smac mimetics used as single agents and these cell lines are at risk of developing drug resistance to Smac mimetics. Thus, it is important to understand the molecular mechanisms underlying intrinsic and acquired resistance of cancer cells to Smac mimetics in order to develop effective therapeutic strategies to overcome or prevent Smac mimetic resistance. We established Smac mimetic resistant sublines derived from MDA-MB-231 breast cancer cells, which exhibit exquisite sensitivity to the Smac mimetic SM-164, and used microarrays to detail the global programme of gene expression underlying SM-164 resistance in MDA-MB-231 cells and identified differentially expressed genes in SM-164-resistant and -sensitive MDA-MB-231 cells. SCID mice with MDA-MB-231 xenograft tumors were treated with 5 mg/kg of SM-164 intravenously for 5 days/week for 2 weeks. SM-164-regressed MDA-MB-231 tumors regrew after treatment ended. Tumor cells from these regrown MDA-MB-231 tumors were isolated and total RNAs were prepared for microarray analysis.

2012-03-01 | E-GEOD-33827 | biostudies-arrayexpress

Gene-expression profiling of ZNF217-overexpressing MDA-MB-231 cells

Project description:To obtain an overview of the cellular functions regulated by ZNF217 signaling in breast-cancer cell lines, we performed global gene-expression profiling on MDA-MB-231-pcDNA6 and MDA-MB-231-ZNF217 cells Two independent cell-culture replicates from the total population of MDA-MB-231-pcDNA6 and MDA-MB-231-ZNF217 stable transfectants were used to generate total RNA. Total RNA was extracted from cell culture using a Qiagen RNA extraction kit and RNA quality was assessed using the BioAnalyzer 2100™ (Agilent Technologies). Complex probes were produced from these RNA, then hybridized to Human genome U133 Plus 2.0 array according to the manufacturer’s recommendations (Affymetrix).

2012-02-06 | E-GEOD-35511 | biostudies-arrayexpress

RNA-seq of mesenchymal stromal cells cultured in the presence of breast cancer cell secretomes

Project description:Mesenchymal stromal cells were cultured in 3D PEG hydrogels for 7 days in the presence of serum-free media or conditioned media from a panel of breast cancer cells (MCF-7, MDA-MB-231, MDA-MB-231 lung-tropic, MDA-MB-231 brain-tropic, MDA-MB-231 bone-tropic). In all cases, the secretomes were collected after cancer cells were in serum-free media for 24h.

2019-05-28 | E-MTAB-6998 | biostudies-arrayexpress

Cancer-cell-secreted miR-9-5p regulates cholesterol homeostasis to promote tumor metastasis [TF TB Rab27AKD miR-9KO]

Project description:To investigate the effects of breast cancer derived EVs on liver metabolism,we inoculated MDA-MB-231,231 /Rab27A KD and 231 /miR-9 KO cells into subcutaneous tumor in NSG mice. We then performed gene expression profiling analysis using data obtained from RNA-seq of liver from mice xenografted MDA-MB-231 cells (tumor bearing) or MDA-MB-231/Rab27A KD cells (231/Rab27A KD) or MDA-MB-231 /miR-9 KO (231/miR-9 KO) and tumor free mice.

2024-08-31 | GSE222707 | GEO

Label-free mass spec analysis of human breast cancer MDA-MB-231 control cells and siICAM1 knockdown

Project description:Human breast cancer MDA-MB-231 cell siControl and siICAM1

2021-05-25 | PXD026234 | JPOST Repository

Proteomics of Triple Negative Breast Cancer Cells Treated with SU056

Project description:1. Quantitative Proteomics: MDA-MB-231, MDA-MB-468, and MCF12A cells were treated with DMSO (vehicle control) or SU056 (novel small molecule drug candidate). Quantitative proteomics analysis was performed on cell lysates. 2. Cellular Thermal Shift Assay (CETSA): MDA-MB-231 cells were treated with DMSO or SU056 and incubated at different temperatures and protein differences in the resulting soluble and insoluble fractions were determined.3. Cellular Thermal Shift Assay (CETSA): MDA-MB-231 YBOX1 KD cells were treated with DMSO or SU056 and incubated at different temperatures and protein differences in the soluble fractions were determined.

2024-04-04 | PXD042380 | Pride

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