Gene expression profile in MCF7 breast cancer cells after 78 functionallly important molecules were knocked down using siRNA.
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Li Wang
PROVIDER: E-GEOD-31912 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:Affymetrix microarray data was generated from MCF7 breast cancer cells treated in vitro with siRNAs against 78 transcription factors and signalling molecules.
2012-03-15 | GSE31912 | GEO
Project description:Affymetrix microarray data was generated from MCF7 breast cancer cells treated in vitro with siRNAs against estrogen receptor alpha (ESR1). Gene expresion of estrogen receptor alpha (ESR1) was knocked down in MCF7 breast cancer cells using siRNA. Then the gene expression profiles of these MCF7 cells, along with non-targetting control treated cells were analysed using Affymetrix Human Genome U133 Plus 2.0 microarrays.
2012-05-06 | E-GEOD-37820 | biostudies-arrayexpress
Project description:Transcriptional profiling of human normal-like breast cells MCF10A comparing control MCF10A cells transfected with a pLenti6/BLOCK-iT™-DEST vector with MCF10A cells transfected with a pLenti6/BLOCK-iT™-DEST vector containing TRIM29 shRNA targeting nucleotides 1265–1285 of the TRIM29 open reading frame (ORF, NM_012101). Transcriptional profiling of human breast cancer cells MCF7 comparing control MCF7 cells transfected with a pLenti6.2/N-LumioTM/V5-DEST vector with MCF7 cells transfected with a pLenti6.2/N-LumioTM/V5-DEST vector containing TRIM29 full-length cDNA (ORF, NM_012101). Two-condition experiment, MCF10A-vector control vs. MCF10A-TRIM29 shRNA cells; MCF7-vector control vs. MCF7-TRIM29 cells.
2010-12-23 | E-GEOD-26238 | biostudies-arrayexpress
Project description:Retinoic acid (RA) triggers growth-suppressive effects in tumor cells and therefore RA and its synthetic analogs have great potential as anti-carcinogenic agents. RA effects are mediated by retinoic acid receptors (RARs), which regulate gene expression in an RA-dependent manner. To define the genetic network regulated by RARs in breast cancer cells, we identified RAR genomic targets using chromatin immunoprecipitation and expression analysis in a model breast cancer cell line MCF-7. Furthermore, we identified genomic binding sites for two putative RAR coregulators FoxA1 and GATA3. Keywords: ChIP-Chip Analysis This series contains ChIP-Chip raw data for four transcription factors (RARA, RARG, FoxA1 and GATA3) in MCF-7 cells. All the experiments are done in triplicates. We mapped the binding sites of RARA, RARG and GATA3 in the bacterial artificial chromosome (BAC) transgenic MCF7 cells in which we tagged the transcription factors with a modified LAP (localization and affinity purification) tag containing green fluorescent protein (GFP). Goat anti-GFP (raised against His-tagged full-length eGFP and affinity-purified with GST-tagged full-length eGFP) was used to perform ChIP experiments in those transgenic lines. To map the binding sites of RARs, MCF7 Cells were hormone-deprived for 3 days and then were treated with 100 nM AM580 (RARA-selective agonist) or 100 nM CD437 (RARG-selective agonist) for 1 hour at 80% confluence. FoxA1 binding sites were mapped using goat anti-FoxA1 antibodies (Abcam: ab5089). Control data include Input from MCF-7 cells. ChIP-Chip experiments with eGFP antibody in wide type MCF-7 cells are used to control eGFP antibody non-specific binding.
2009-03-16 | E-GEOD-15244 | biostudies-arrayexpress
Project description:To identify the target of miR-212, miR-132 and HIC1, we have employed whole genome microarray expression profiling on the human breast cancer MCF7 cells. To generate miR-212/132 or HIC1 inducible MCF7 cells, doxycycline-dependent miR-212/132 or HIC1 gene expression system was used. Either Tet-ON miR-212/132 MCF7 or Tet-ON HIC1 MCF7 were treated with 1μg/ml of Doxycycline for 36 hours with EMEM containing 0.01 mg/ml bovine insulin and 10% FCS. Two independent experiments were performed.
2014-07-29 | E-GEOD-37945 | biostudies-arrayexpress
Project description:We have devised a technology that enables chromatin immunoprecipitation (ChIP) experiments in cultured human cells by circumventing both the laborious production of protein-specific antibodies and the optimization of crosslinking/immunoprecipitation conditions for each protein. Our approach utilizes bacterial artificial chromosomes (BACs) to physiologically express chromatinbinding proteins fused to epitope tags that are recognized by widely available and highly specific antibodies. We demonstrate the robustness of our methodology for mapping chromatin binding sites of transcription factors. Keywords: ChIP-Chip Analysis This series contains ChIP-on-Chip data sets for three transcription factors (FOXA1 (Forkhead box A1), XBP1-S (spliced X-box binding protein 1) and VDR (Vitamin D receptor)) and control samples (INPUT) for partial of the human genome including chromosomes 4, 15, 18, and 20 in MCF7 cells. We mapped the binding sites of these three transcription factors in the BAC transgenic MCF7 cells in which we tagged the transcription factors with a modified LAP (localization and affinity purification) tag. Goat anti-GFP (raised against His-tagged full-length eGFP and affinity-purified with GST-tagged full-length eGFP) was used to perform ChIP experiments in those transgenic lines. For comparison, we also mapped FOXA1 and XBP1-S binding sites with the available antibodies against the endogenous proteins. Goat anti-FoxA1 (Abcam: ab5089) and goat anti-XBP1 (Santa Cruz Biotech: sc-7160X) were used in these studies. Independent biological triplicates were performed for each transcription factor, as well as the control (Input).
2010-05-25 | E-GEOD-10845 | biostudies-arrayexpress
Project description:Insulin analogues are designed to improve the pharmacokinetic parameters compared to regular human insulin. This provides a sustained control of blood glucose levels in diabetic patients. All novel insulin analogues are tested for their mitogenic side effects, however these assays do not take into account the molecular mode-of-action of different insulin analogues. Insulin analogues can bind the insulin receptor (INSR) and the insulin-like growth factor-1 receptor (IGF1R) with different affinities and consequently will activate different downstream signaling pathways. Here we used a panel of MCF7 human breast cancer cell lines that selectively express either one of the isoforms of the INSR (IRA or IRB) or the IGF1R. We sought to study the role of the different receptors (IRA, IRB and IGF1R) in the mitogenic signaling of insulin-like molecules (including insulin, glargine, X10 (or AspB10) and IGF1). MCF7 IRA, MCF7 IRB or MCF7 IGF1R cells (as described in Arch Toxicol. 2014 Apr;88(4):953-66. doi: 10.1007/s00204-014-1201-2. Epub 2014 Jan 25.) were cultured in RPMI supplemented with 5% (v/v) CDFBS (Hyclone) and used for experiments. Cells have been exposed for 1 or 6 hours to 10 nM of the indicated insulin-like molecule. As a control sample a vehicle stimulation was performed that contained everything except the active compound.
2015-01-29 | E-GEOD-65398 | biostudies-arrayexpress
Project description:Novel mass spectrometry (MS)-based proteomic tools with extremely high sensitivity and high peak capacity are required for comprehensive characterization of protein molecules in mass-limited proteome samples. We previously reported a nanoflow RPLC-CZE-MS/MS (nanoRPLC-CZE-MS/MS) system for deep bottom-up proteomics of low micrograms of human cell samples (Yang et al. Anal. Chem. 2018, 90, 10479-10486). In this work, we further improved the sensitivity of the nanoRPLC-CZE-MS/MS system drastically via employing bovine serum albumin (BSA) treated sample vials, improving the nanoRPLC fraction collection procedure, and using a shorter capillary for fast CZE separation. The improved nanoRPLC-CZE produced a high peak capacity of 8500 for peptide separation. The improved system identified 6500 proteins from a MCF7 proteome digest starting with only 500-ng peptides using a Q-Exactive HF mass spectrometer. The system actually consumed roughly 100-ng peptides. The improved system produced a comparable number of protein identifications (IDs) to our previous system with 10-fold less sample consumption. The improved system is also comparable to the two-dimensional (2D) nanoRPLC-MS/MS system developed by the Mann’s group regarding the number of protein IDs starting with 500-ng human cell proteome digests but with 4-fold lower sample consumption. We further coupled single spot solid phase sample preparation (SP3) method to the improved nanoRPLC-CZE-MS/MS for bottom-up proteomics of 5000 HEK293T cells, resulting in 3689 protein IDs with the consumption of a peptide amount that corresponded to only roughly 1000 cells. This work represents the first study of a small number of human cells using CZE-MS/MS.
2019-10-23 | PXD014392 | Pride
Project description:Proteome profile of MCF7 breast cancer cells stimulated with insulin and analyzed by nano-LC-ESI-MS/MS.
2016-11-30 | PXD004051 | Pride
Project description:Estrogens are steroid hormones that play critical roles in the initiation, development, and metastasis of breast and uterine cancers. The estrogen (E2) response in breast cancer cells is predominantly mediated by the estrogen receptor-alpha (ER alpha), a ligand-activated transcription factor. ER alpha regulates transcription of target genes through direct binding to its cognate recognition sites, known as estrogen response elements (EREs), or by modulating the activity of other DNA-bound transcription factors at alternative DNA sequences. The proto-oncogene c-myc is upregulated by ER¦à in response to E2 and encodes a transcription factor, c-MYC, which regulates a cascade of gene targets whose products mediate cellular transformation. This study aims at mapping the binding sites of these two transcription factors (ER alpha and c-MYC) in one ER alpha positive breast cancer cell line (MCF7 cell line). Keywords: ChIP-Chip Analysis This series contains ChIP-on-Chip data sets for two transcription factors (ER alpha and c-MYC) and control samples (INPUT). All the experiments are done in triplicates. MCF7 Cells were E2-deprived for 3 days and then were treated with 10 nM E2 (45 minutes and 2 hours for mapping ER alpha and c-MYC binding sites, respectively) at 80% confluence.
2010-05-26 | E-GEOD-10800 | biostudies-arrayexpress