Expression data from ALK over-expressed MCF-7 clones and control clones
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Annie Luo
PROVIDER: E-GEOD-41635 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:To evaluate the function of ALK in breast cancer, we enforcing expressed full length wild type ALK in the parental MCF-7 breast cancer cell line that we have established in previous studies have a very low invasive capacity, do not form tumor emboli nor do they invade into the dermal lymphatics when grown as xenografts.
2012-10-17 | GSE41635 | GEO
Project description:Human breast cancer cell line MCF-7 is usually sensitive to chemotherapy drug BMS-554417, an insulin receptor (IR) and insulin-like growth factor receptor (IGFR) inhibitor. However, through step-wise increase in BMS-554417 doses in culture media, we were able able to screen and select a single MCF-7 clone that is BMS-554417 resistant. It is cross resistant to BMS-536924. This new line of MCF-7 cells was named as MCF-7R4. The transcriptome profiling of both MCF-7 and MCF-7R4 was performed using Affymetrix HG-U133 plus2.0 GeneChip arrays. Five replicates of MCF-7 and five replicates of MCF-7R4 were profiled.
2009-11-05 | E-GEOD-18912 | biostudies-arrayexpress
Project description:TGFBR1*6A is a common hypomorphic variant of the type 1 Transforming Growth Factor Beta Receptor (TGFBR1), which has been associated with increased cancer risk in some studies. Although TGFBR1*6A is capable of switching TGF-β growth inhibitory signals into growth stimulatory signals when stably transfected into MCF-7 breast cancer cells, TGFBR1*6A biological effects are largely unknown. To broadly explore TGFBR1*6A potential oncogenic properties, we assessed its impact on the migration and invasion of MCF-7 cells. We found that TGFBR1*6A significantly enhances MCF-7 cell migration and invasion in a TGF-β signaling independent manner. We set up and performed a gene array using the conditions mimicking the cell migration experiments to determine which genes in the migratory pathway were differentially regulated between the MCF-7*6A cells and the MCF-7*9A (wild type transfected) cells. The gene array identified two downregulated genes in *6A compared to *9A that are involved in cell migration and invasion: ARHGAP5, encoding ARHGAP5, and FN1, encoding fibronectin-1 (FN1). We were subsequently able to use this information in further studies in the lab. Experiment Overall Design: MCF-7 cells were stably transfected with pIRES-TGFBR1-HA-FLAG or pIRES-TGFBR1*6A-HA-FLAG. Clones were picked up and named 6A-SA5 and WT-WB1 referring to the *6A and TGFBR1 clones, respectively. We have found that the *6A mutation causes an increase in migration and invasion of MCF-7 cells which is independent of TGF-beta. We used the gene array to identify genes that were differentially regulated between the two cell lines that could lead to this phenotype. We collected RNA from samples that were serum-deprived overnight prior to being fed with complete media to mimic the conditions in the migration experiment. No exogenous growth factors were added to the media besides the normal 10% heat inactivated FBS. Samples were collected and run in triplicate (referred to in this data set as sample 1, sample 2, and sample 3). The âuntreatedâ refers to the fact that samples were grown in complete media alone with no exogenously added growth factors.
2008-11-22 | E-GEOD-9093 | biostudies-arrayexpress
Project description:The human steroid receptor RNA activator (SRA) gene encodes both non-coding RNAs (ncRNAs) and protein-generating isoforms. However, the breadth of endogenous target genes that might be regulated by SRA RNAs remains largely unknown. To address this, we depleted SRA RNA in two human cancer cell lines (HeLa and MCF-7) with small interfering RNAs, then assayed for changes in gene expression by microarray analyses using Affymetrix HGU133+2 arrays. We also tested if SRA depletion affects estradiol-regulated genes in MCF-7 breast cancer cells. We transiently transfected HeLa or MCF-7 human cancer cell lines with with non-targeting (NT) or SRA-targeting siRNAs. Six total HeLa RNA samples were analyzed on an Affymetrix HGU133+2 array, representing three biological triplicates. Likewise, 12 total MCF-7 RNA samples were analyzed on Affymetrix HGU133+2 arrays, representing biological trilplicates for both NT and siSRA transfected cells and with/without 10 nM estradiol (E2) for 6 hours.
2010-02-21 | E-GEOD-20081 | biostudies-arrayexpress
Project description:Human breast cancer cells MDA-MB-435 had higher metastatic potential and other aggressive characteristics than MCF-7 cells. Next-generation RNA sequencing (RNA-Seq) was used to clear this concern through comparison the transcriptomic expression profiles of these two cells. Total RNA were extracted from MCF-7 and MDA-MB-435S cells, and the polyA+ mRNA was sequenced using Illumina Genome Analyzer IIx. The reads were mapped to RefSeq RNA reference sequences.
2014-01-17 | E-GEOD-54122 | biostudies-arrayexpress
Project description:Developing effective model systems to evaluate new potential chemotherapeutic reagents is critical. Three-dimensional cell cultures, such as spheroids, aid in bridging the gap between commonly used monolayer cell cultures and significantly more complex and expensive animal models. Spheroid model systems contain pathophysiological and chemical gradients similar to an in vivo tumor, which ultimately form distinct cellular subpopulations. In the spatial SILAC model, labels are pulsed into the spheroid at discrete time windows during development. These media pulses result in labeled proteins in distinct regions of the spheroid, which allows for tracing of quantitative proteomic changes to be correlated to different cellular subregions. In this study, we use the Spatial SILAC model to evaluate the proteomic response of a colon carcinoma spheroid to the multikinase inhibitor Regorafenib. We determined regorafenib to be an effective kinase inhibitor which significantly altered whole spheroid proliferation and resulted in increased apoptosis when the signal was averaged for all cells in the culture. However, when regorafenib treatment is more closely examined among the cellular subpopulations, drastic differences are observed for how the drug impacted the proteome of the necrotic spheroid core and the proliferating outer regions. Whole spheroid and outer region analysis shows that regorafenib treatment inhibited critical pathways such as mTOR signaling, ERK/MAPK signaling, and colorectal cancer metastasis signaling. However, analysis of the core shows that regorafenib had an entirely different effect, including upregulation of MAPK1 and KRAS, possibly indicating drug resistance within these late apoptotic cells. Ultimately, these combinatory studies can be used to further understanding of drug metabolism is different cellular subpopulations and provide valuable information to ultimately improve the accuracy of therapeutic testing.
2024-08-09 | PXD038958 | Pride
Project description:The long-term goal of our study is to understand the genetic and epigenetic mechanisms of breast cancer metastasis in human and to discover new possible genetic markers for use in clinical practice. We have used microarray technology (Human OneArray microarray, phylanxbiotech.com) to compare gene expression profiles of non-invasive MCF-7 and invasive MDA-MB-231 cells exposed to dioscin (DS), a steroidal saponin isolated from the roots of wild yam, (Dioscorea villosa). Initially the differential expression of genes (DEG) was identified that followed pathway enrichment analysis (PEA). Of the genes queried on OneArray, we identified 4641 DEG changed between MCF-7 and MDA-MB-231 cells (vehicle-treated) with cut-off log2 |fold change|⧠1. Among these genes, 2439 genes are upregulated and 2002 genes are downregulated. DS exposure (2.30 ïM, 72 h) to these cells identified 801 (MCF-7) and 96 (MDA-MB-231) DEG that showed significant difference compared to untreated cells (p<0.05). Within these gene sets, DS is able to upregulate 395 genes and downregulate 406 genes in MCF-7 and upregulate 36 and downregulate 60 genes in MDA-MB-231 cells. Further comparison of DEG between MCF-7 and MDA-MB-231 cells exposed to DS identified 3626 DEG of which 1700 were upregulated and 1926 genes were down-regulated. From PEA, 12 canonical pathways were significantly altered between these two cell lines (MCF-7 and MDA-MB-231). However, no alteration in any of these pathways was noticed in MCF-7 cell, while in MDA-MB-231 cells only MAPK pathway showed significant alteration. When PEA comparison was made on DS exposed cells, it was observed that only 2 pathways were significantly affected. Further, to identify shared DEG, which are targeted by DS and overlapped in both MCF-7 and MDA-MB-231 cells, we performed intersection analysis (Venn diagram). We found that only 7 DEG are overlapped of which six are reported in the database. This study highlights the diverse gene networks and pathways through which DS exhibits its effect on breast cancer cells. Two condition experiment. Human breast cancer Cell line MCF-7 groups: Vehicle control and dioscin treated; Human breast cancer cell line MDA-MB-231 cell group; vehicle control and dioscin-treated. Biological replicates: MCF-7 control compared to MCF-7 dioscin treated; MDA-MB-231 control compated to MDA-MB-231 dioscin-treated; MCF-7 control compared to MDA-MB-231 control; MCF-7 dioscin treated compared to MDA-MB-231 dioscin-treated. duplicate array
2016-03-22 | E-GEOD-79465 | biostudies-arrayexpress
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Project description:Methylated DNA binding protein 2 (MBD2) has been shown to bind specific methylated promoters and suppress transcription. Here we systematically investigate MBD2 suppression by overexpressing MBD2 in MCF-10A cells and generating gene expression profiles of overexpressing cells and normal MCF-10A cells. MCF-10A cells were infected with MBD2 lentivirus in order to increase MBD2 expression. Total RNA was extracted from both infected and non-infected cells and hybridized to Affymetrix gene expression microarrays. Three technical replicates were hybridized for infected and non-infected cells.
2013-06-17 | E-GEOD-47873 | biostudies-arrayexpress