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Expression data for T47D cells treated with 2mM hydroxyurea

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

SUBMITTER: Jessop Lea

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

REPOSITORIES: biostudies-other

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Expression data for T47D cells treated with 2mM hydroxyurea

2014-04-22 | GSE56940 | GEO

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.

2014-04-22 | E-GEOD-56940 | biostudies-arrayexpress

Expression data with either EglN2 or control knockdown in T47D cells

Project description:In order to perform integrated analysis for EglN2 ChIP-Seq and microarray to identify EglN2 direct target genes, we performed the microarray analysis for T47D breast cancer cells with either control or EglN2 siRNA followed by hypoxia+DMOG treatment T47D cells were transfected with either control or EglN2 siRNA in duplicate with RNAi max. 36 hours following transfection, cells were treated with hypoxia (1%) and DMOG (1 mM) for 16 hours. Following treatment, total RNA was extracted using Rnaeasy kit from Qiagen.

| S-ECPF-GEOD-59936 | biostudies-other

Twist expression in HMLE and breast cancer T47D cells

Project description:Twist is a key EMT inducer, expression of Twist will induce EMT in HMLE and breast tumor T47D cells By expressing Twist in HMLE and T47D cells, which lack the expression of Twist, will identify the genes regulated by Twist Expressing Twist in HMLE and T47D cells, stable clones were selected and treated with BET inhibitor JQ1 and RNA were prepared for microarray analysis

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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

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Effect of tamoxifen on early gene expression in T47D cells

Project description:Tamoxifen is the treatment of choice in estrogen receptor alpha breast cancer patients. However, ~50% of ERα-positive tumors exhibit intrinsic or rapidly acquire resistance to endocrine treatment, requiring chemotherapy. Ιt has been difficult to predict de novo resistance to endocrine therapy and/or assess the likelihood of early relapse, while no concrete mechanism regulating the acquisition and the maintenance of endocrine resistance has been identified. We have performed a whole transcriptome analysis of an ER-positive (T47D) and a triple-negative (MDA-MBA-231) breast cancer cell line exposed to tamoxifen for a short time frame (hours) in order to study resistance mechanisms that are initiated early after initiation of tamoxifen treatment. Cells after a 4h incubation with medium containing 10% charcoal stripped FBS were incubated with vehicle, E2 (10-6M) or tamoxifen (10-6M) in RPMI 1640 supplemented with 10% charcoal stripped FBS, for 3 hours. Total RNA was isolated using Nucleospin II columns (Macheray-Nagel, Dttren, Germany), according to the manufacturer’s instructions. RNA was labeled and hybridized according to the Affymetrix protocol (Affymetrix Gene-Chip Expression Analysis Technical Manual), using the HGU133A plus 2 chip, analyzing a total of 54675 transcripts. Signals were detected by an Affymetrix microarray chip reader.

| S-ECPF-GEOD-60878 | biostudies-other

Proviral structure, chromosomal location, and expression of HERV-K-T47D, a novel human endogenous retrovirus derived from T47D particles.

Project description:We previously described that type B retrovirus-like particles released from the human mammary carcinoma cell line T47D are pseudotypes and package retroviral RNA of different origins (W. Seifarth, H. Skladny, F. Krieg-Schneider, A. Reichert, R. Hehlmann, and C. Leib-Mösch, J. Virol. 69:6408-6416, 1995). One preferentially packaged retroviral sequence, ERV-MLN, has now been used to isolate the corresponding full-length provirus from a human genomic library. The 9,315-bp proviral genome comprises a complete retroviral structure except for a 3' long terminal repeat (LTR) truncation. A lysine tRNA primer-binding site and phylogenetic analyses assign this human endogenous retroviral element, now called HERV-K-T47D, to the HML-4 subgroup of the HERV-K superfamily. The gag, prt, pol, and env genes exhibit 40 to 60% amino acid identity to HERV-K10. HERV-K-T47D is located on human chromosome 10, with five closely related elements on chromosomes 8, 9, 15, 16, and 19 and several hundred HERV-K-T47D-related solitary LTRs dispersed over the human genome. HERV-K-T47D-related sequences are detected in the genomes of higher primates and Old World monkeys but not in those of New World monkeys. High HERV-K-T47D transcription levels were observed in human placenta tissue, whereas transcription in T47D cells was strictly steroid dependent.

| S-EPMC110222 | biostudies-literature

Tn-seq of hydroxyurea treated Bacillus subtilis cells

Project description:Hydroxyurea (HU) is thought to primarily target ribonucleotide reductase (RNR), therefore inhibiting the conversion of rNTPs into dNTPs and slowing DNA replication. To understand how Bacillus subtilis responds to HU stress, we performed RNA-seq and Tn-seq. We obtained genes with fitness defects following hydroxyurea treatment over 3 growth periods.

2021-03-29 | GSE169564 | GEO

RNA-seq of hydroxyurea treated Bacillus subtilis cells

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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.

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