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Expression data from AsPC1 cells treated with ICG-001

ABSTRACT: The CREB binding protein inhibitor ICG-001 suppresses pancreatic cancer growth We used microarrays to detail global gene expression changes in the pancreatic cancer cell line AsPC1 following treatment with ICG-001 or siRNA-mediated knockdown of CTNNB1 (beta-catenin) AsPC1 cells were treated with 10uM ICG-001 or vehicle control (DMSO) for either 6 hours or 24 hours. AsPC-1 cells were also separately transfected with 20nM control siRNA or CTNNB1 siRNA for 48 hours. RNA was extracted at these time points for hybridization to Affymetrix microarrays

ORGANISM(S): Homo sapiens

SUBMITTER: Dawson David

PROVIDER: S-ECPF-GEOD-57728 | biostudies-other |

REPOSITORIES: biostudies-other

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Expression data from AsPC1 cells treated with ICG-001

2014-07-15 | GSE57728 | GEO

Expression data from AsPC1 cells treated with ICG-001

Project description:The CREB binding protein inhibitor ICG-001 suppresses pancreatic cancer growth We used microarrays to detail global gene expression changes in the pancreatic cancer cell line AsPC1 following treatment with ICG-001 or siRNA-mediated knockdown of CTNNB1 (beta-catenin) AsPC1 cells were treated with 10uM ICG-001 or vehicle control (DMSO) for either 6 hours or 24 hours. AsPC-1 cells were also separately transfected with 20nM control siRNA or CTNNB1 siRNA for 48 hours. RNA was extracted at these time points for hybridization to Affymetrix microarrays

2014-07-15 | E-GEOD-57728 | biostudies-arrayexpress

Expression data for T47D cells treated with 2mM hydroxyurea

Project description:RAD51B, a paralog of RAD51, have been associated with breast cancer risk in genome-wide association studies. The underlying biological mechanism through which germline genetic variation in RAD51B confers susceptibility to breast cancer is not well understood. Here we investigate the molecular function of RAD51B in breast cancer cell lines. We used microarrays to detail the global gene expression to identify classes of genes that are regulated differnetly post DNA damages as a result of RAD51B depeletion. T47D cells were first transfected with either non-targeting (control; siCON) or RAD51B-targeting (experimental; siRAD51B) siRNA, then followed by 24hr treatment of 2mM hydroxyurea (HU). Total RNA were extracted at the end of the treatment for microarray analysis. Three biological replicates were carried out for both control and experimental samples.

| S-ECPF-GEOD-56940 | biostudies-other

Expression data from TGFbeta-treated control or aPKC silenced A549 cells

Project description:Aberrant TGFbeta signalling is a hallmark of epithelial derived tumours. Signalling patterns can depend on the membrane trafficking and internalization of the TGFbeta receptors. Protein kinase C (PKC), particularly the atypical PKC isoforms, alter the trafficking of TGFbeta receptors and can alter TGFbeta induced gene expression. We used microarrays to detail the programme of gene expression underlying TGFbeta induction between control or aPKC silenced A549 cells. Control or aPKC silenced A549 cells were serum starved and treated with TGFbeta for 1 hour. Total RNA was extracted from untreated or TGFbeta treated cells after 8 and 24 hours and analyzed using Affymetrix microarrays. We sought to assess TGFbeta gene expression in aPKC silenced lung cancer cells, as we found that knockdown of aPKC extends TGFbeta signalling as assessed by phospho Smad2 levels. Furthermore, increased expression and oncogenic activity of aPKC (PKCiota) has been reported in lung cancer cells.

| S-ECPF-GEOD-26241 | biostudies-other

Expression data from MCF7 and LTED cells treated with YC-1

Project description:To identify novel therapeutic opportunities for patients with acquired resistance to endocrine treatments in breast cancer, we applied high-throughput screening to explore currently marketed drugs. The Ec50 values were determined for MCF7 and LTED cell lines to identify the compounds showing higher inhibition of LTED cells. The best compound was YC-1 and gene microarray studies were done in vitro for mechanistic exploration. MCF7 and LTED cells were treated with YC-1 for RNA extraction and hybridization on Affymetrix microarrays.

| S-ECPF-GEOD-38829 | biostudies-other

Expression data from JQ1 (0.2 uM) treated tamoxifen-resistant MCF7 cells

Project description:Estrogen signaling pathway is critical for breast cancer development and has remained the major adjuvant therapeutic target for this disease. Tamoxifen has been used in clinic for many years to treat ER-positive breast cancer. However a great many (30%) suffer relapse due to drug resistance. In this study, the bromodomain inhibitor JQ1 was found to down-regulate ERalpha gene expression and have anti-tumor effect in cultured tamoxifen-resisant breast cancer cells. We used microarrays to detail the global programme of gene expression in tamoxifen-resistant MCF7 cells treated with the bromodomain inhibitor JQ1. Tamoxifen-resistant breast cancer MCF7 cells were treated with DMSO (vehicle) or JQ1 (0.2 uM) for 24 hours before total RNA was purified for microarray. Each sample was triplicated.

| S-ECPF-GEOD-49124 | biostudies-other

Expression data of MCF-7 cells treated with gamma tocotrienol (g-T3)

Project description:Gamma tocotrienol induces apoptosis in breast cancer cells however, the molecular mechanisms are not completely understood. We used microarrays to detail the global programme of gene expression underlying the effects of gamma tocotrienols on MCF-7 cells and identified distinct classes of up-regulated genes during this process. MCF-7 cells were grown in DMEM medium with 5% FBS. The cells were treated with vehicle control (DMSO) or 40 uM of gamma tocotrienol for 24 h for RNA extraction and hybridization on Affymetrix microarrays. Four independent experiments were performed.

| S-ECPF-GEOD-21946 | biostudies-other

Expression data from BRAFV600E A375 melanoma cells treated with vehicle or vemurafenib

Project description:Vemurafenib is a BRAF inhibitor with specificity for the most common BRAF mutant encountered in melanomas (BRAFV600E). Vemurafenib suppresses the proliferation of BRAF mutant human melanoma cells by suppressing downstream activation of the MEK/ERK mitogen activated protein kinases. We used microarrays to examine the transcriptional response of a vemurafenib-sensitive BRAFV600E human melanoma cell line (A375) to vemurafenib in order to further delineate the mechanisms by which BRAFV600E drives cell proliferation and energy metabolism in human melanoma. BRAFV600E A375 human melanoma cells were treated with vehicle (0.1% DMSO) or 10 uM vemurafenib for 24 h after which total RNA was extracted. Cells were prepared and RNA was extracted in 3 separate batches (three different cell stocks on three separate days) providing three independent replicates (n=3). Paired replicates (prepared from the same stock of cells on the same day) are denoted by A, B and C.

| S-ECPF-GEOD-42872 | biostudies-other

Gene expression data from MCF-7 cells treated with Lacciac Acid A

Project description:Lacciac Acid A was indentified as an inhibitor of DMNT1. MCF-7 cells were treated with Lacciac Acid A (200 uM) for 5 days. Changes in gene expression were identified by using Affymetrix Human gene ST1.0 arrays. We used microarrays to determine global changes in gene expression upon treatment with Lacciac Acid A an inhibitor of DMNT1. MCF-7 cells near mid passage were treated with Lacciac Acid A for 5 days. RNA was extracted and hybridized on Affymetrix microarrays. Treated and untreated cells were from the same cell passage. Two sample sets from the same passage and the third set from the previous passage were used.

| S-ECPF-GEOD-45804 | biostudies-other

Expression data analyzed with LPIA in A549 lung carcinoma cells treated with geldanamycin

Project description:The statsitcal model, latent pathway identification analysis (LPIA), was implemented for the analysis of A549 lung carcinoma cells treated with geldanamycin. Control and treated samples were assayed with Affymetrix HG_U133_plus_2 arrays and analyzed using LPIA. LPIA looks for statistically signﬁcant evidence of dysregulation in a network of pathways constructed in a manner that explicitly links pathways through their common function in the cell. Geldanamycin (geld) is known to inhibit the molecular chaperone protein, Hsp90, and plays a role in preventing the malignant transformation and proliferation of healthy cells during oncogenesis. LPIA successfully identified pathways specific to geldanamycin effects at the gene transcription level. A549 lung carcinoma cells were allowed to adhere for 24h and further incubated in the presence of geldanamycin at a concentration equivalent to the determined IC50 of 40 nM or IC20 of 10 nM, or with vehicle DMSO (final concentration 0.4%). After 24h and 48 h, cells were harvested and total RNA was purified and processed for Affymetrix HG_U133_Plus_2.0 microarray analysis. Raw probe intensities were RMA-normalized and avereaged for three replicates for each condition. Probe sets for 54,120-annotated open reading frames were included in LPIA analysis.

| S-ECPF-GEOD-26525 | biostudies-other

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