Expression data in MDA-MB-231 cells treated with siATM, sip53 or control (SiNC) siRNA
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Wei-Ta Chen
PROVIDER: E-GEOD-60479 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:The purpose of this microarray experiment was to obtain reference gene expression patterns of a number of epithelial cell populations [mammary stem cells (MASC), luminal progenitors (LP), alveolar luminal stem/progenitor cells (WC virgin-these are mammary epithelial cells genetically marked by Wap-Cre in virgin females), mature luminal cells (ML, mainly represent ductal luminal cells in virgin females), and alveolar luminal cells (WC preg M-bM-^@M-^S these are alveolar cells genetically marked by Wap-Cre during mid-gestation)] present in the mammary gland of wildtype adult mice on a C57BL6 genetic background. For the isolation of RNA from mammary stem cells (MASC, Lin-CD24+CD29hi), luminal progenitors (LP, Lin-CD24hiCD29+CD61+), and mature luminal cells (ML, lin-CD24hiCD29+CD61-), the thoracic and inguinal mammary glands from 3 adult virgin female mice were harvested, minced and digested into a single cell suspension. Form each of these 3 single cell suspensions, the above populations were sorted by FACS. For alveolar luminal stem/progenitor cells and alveolar luminal cells, Lin-YFP+ mammary epithelial cells were isolated from virgin or midgestation mice genetically marked by Wap-Cre;R26Y. R26Y is a conditional YFP reporter that would be turned on upon Cre-mediated recombination.
2014-11-26 | E-GEOD-47376 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series
2014-11-26 | E-GEOD-47377 | biostudies-arrayexpress
Project description:RUNX1 encodes a RUNX family transcription factor (TF) and was recently identified as a novel mutated gene in human luminal breast cancers. We found that Runx1 is expressed in all subpopulations of murine mammary epithelial cells (MECs) except the secretory alveolar luminal cells. Conditional knockout of Runx1 in MECs by MMTV-Cre led to a decrease in luminal MECs, largely due to a profound reduction in the estrogen receptor (ER)-positive mature luminal subpopulation, a phenotype that could be rescued by loss of either Trp53 or Rb1. Mechanistically RUNX1 represses Elf5, a master regulatory TF gene for alveolar cells, and activates Foxa1, a key mature luminal TF gene involved in the ER program. Collectively, our data identified a key regulator of the ER+ luminal lineage whose disruption may contribute to development of ER+ luminal breast cancer when under the background of either TP53 or RB1 loss. Thoracic and inguinal mammary glands from 3 MMTV-Cre;Runx1L/L;R26Y and 3 MMTV-Cre;Runx1+/+;R26Y adult virgin females were dissected out, minced and digested to single cell suspension. Runx1L is the floxed conditional knockout allele of Runx1. R26Y is a conditional YFP reporter that would be turned on upon Cre-mediated recombination. FACSaria machine was used to sort out the YFP-marked luminal epithelial cell population of each of these 6 mice. Total RNA was isolated with Qiagen RNeasy kit and subsequently amplified by Nugen V2 and applied to Affymetrix mouse genome 430 2.0 arrays.
2014-11-26 | E-GEOD-47375 | biostudies-arrayexpress
Project description:TMPRSS2-ERG gene fusions that are frequently identified in prostate cancer can be generated either through chromosomal translocation or via interstitial deletion. The latter mechanism deletes an interstitial region of ~3Mb and it remains largely unanswered whether genes deleted within this region contribute to prostate cancer. By characterizing two knockin mouse models recapitulating TMPRSS2-ERG fusions with or without the interstitial deletion, we found that only those with deletion developed poorly differentiated adenocarcinomas with epithelial-to-mesenchymal transition, when under a Pten-null background. We identified several interstitial genes, including ETS2 and BACE2, whose reduced expression correlates with worse disease-free survival and lethal disease. By using an Ets2 conditional knockout allele, we demonstrated that loss of one copy of Ets2 was sufficient for prostate cancer progression when under a Pten-null background. Collectively, our data suggest that ETS2 is a prostate tumor suppressor and haploinsufficiency of one or more interstitial genes contributes to prostate cancer progression. Genotyped male mice were euthanized at 12 months of age and prostates isolated. Prostates were fixed overnight in 10% formalin and stored in 70% ethanol until tissue processing and paraffin embedding. Serial sections were cut from paraffin blocks which were stained for H&E and analyzed by a trained rodent histopathologist. Using these sections as a visual guide for specific types of lesions, the sequential sections were stained with hematoxylin and used for laser capture microdissection on ArcturusXT system. Epithelial cells within notable high grade prostate intraepithelial neoplasia (HG-PIN) lesions were microdissected from 3 mice from each corresponding genotype. In addition, poorly differentiated adenocarcinomas from PbCre;T-3Mb-Erg/+;PtenL/L mice were also dissected. RNA was isolated from the microdissected tissue using the Qiagen RNeasy FFPE kit and subjected to Nugen Amplification before microarray analysis on an Affymetrix Mouse Gene 2.0 ST chip.
2015-12-31 | E-GEOD-63070 | biostudies-arrayexpress
Project description:Functional analysis of ABCB5 in A375 and G3361 melanoma cells, by comparing stably-transfected controls to ABCB5-shRNA-targeted cells. 12 samples total. Replicates n=3 for the following 4 groups: A375 pSUPER-retro-puro-Vector vs. A375 pSUPER-retro-puro-ABCB5-KD; G3361 pSUPER-retro-puro-shCNTRL vs. G3361 pSUPER-retro-puro-ABCB5-KD.
2014-06-17 | E-GEOD-38290 | biostudies-arrayexpress
Project description:The NKX2-1 transcription factor, a regulator of normal lung development, is the most significantly amplified gene in human lung adenocarcinoma. To better understand how genomic alterations of NKX2-1 drive tumorigenesis, we generated an expression signature associated with NKX2-1 amplification in human lung adenocarcinoma, and analyzed DNA binding sites of NKX2-1 by genome-wide chromatin immunoprecipitation from NKX2-1-amplified human lung adenocarcinoma cell lines. Combining these expression and cistromic analyses identified LMO3, itself encoding a transcription regulator, as a candidate direct transcriptional target of NKX2-1, in addition to consensus binding motifs including a nuclear hormone receptor signature and a Forkhead box motif in NKX2-1-bound sequences. RNA interference analysis of NKX2-1-amplified cells compared to non-amplified cells demonstrated that LMO3 mediates cell proliferation downstream of NKX2-1; cistromic analysis that NKX2-1 may cooperate with FOXA1. Our findings provide new insight into the transcriptional regulatory network of NKX2-1 and suggest that LMO3 is a transducer of lineage specific cell survival of NKX2-1-amplified lung adenocarcinomas. NCI-H2009 cells with stable expression of either pLKO-Tet-Op-shGFP (n=4) or pLKO-Tet-Op-shNKX2-1 (pooled population; n=3 and a clone; n=3) were treated with 50ng/ml of doxycyline for 48 hours. Total RNA was extracted, gene expression profiling was performed and differential gene expression between shGFP and shNKX2-1 was analyzed to determine the effects by suppression of NKX2-1 in NCI-H2009 cells.
2013-04-15 | E-GEOD-40270 | biostudies-arrayexpress
Project description:Primary rib chondrocyte were isoloated from P0.5-day old wildtype and Col2-Cre:floxed EED conditional knockout mouse pups,and cultured overnight in 10%FCS containing DMEM. RNA was isolated and subjected to Affymetrix Mouse Gene ST 1.0 array. Primary rib chondrocyte were isoloated from P0.5-day old wildtype and Col2-Cre:floxed EED conditional knockout mouse pups,and cultured overnight in 10%FCS containing DMEM. RNA was isolated and subjected to Affymetrix Mouse Gene ST 1.0 array. Biological duplicate. Mice were in a mixed genetic background of C57/B6 and 129sv.
2015-11-01 | E-GEOD-66862 | biostudies-arrayexpress
Project description:NLRC5 is a member of the NLR family of proteins. The observation that NLRC5 is found in the nucleus prompted us to perform a gene array to identify putative target genes of NLRC5. We generated Jurkat T cell lines that stably express either the wild-type or mutant forms of NLRC5 harboring mutations in the nucleotide binding domain (NBD): Walker A (deficient in nucleotide binding), Walker B (deficient in nucleotide hydrolysis), and the combined Walker AB, carrying both mutations. Site-directed mutagenesis was used to create the NLRC5 NBD mutants: Walker A (K234A), Walker B (E311Q), and Walker AB (both mutations). We compared the expression profiles of Jurkat T cells expressing GFP, or the GFP-tagged wild-type, Walker A, Walker B, or Walker AB forms of NLRC5. GFP and the Walker A and Walker AB forms of NLRC5 were considered functionally inactive, while the wild-type and Walker B forms of NLRC5 were considered functionally active. These groups were used as biological replicates to assess the effect of NLRC5 activity on gene expression.
2010-07-30 | E-GEOD-22064 | biostudies-arrayexpress
Project description:Bronchial asthma is associated with type 2 immune responses induced by components of adaptive as well as innate immunity. Although innate cytokines such as IL-25 have been shown to play key roles in development of airway hyperreactivity (AHR), little is known of innate molecules that regulate IL-25-mediated airway inflammation. We found that blockade of repulsive guidance molecule b (RGMb) in an experimental murine model of asthma blocked the development of AHR, a cardinal feature of asthma, and that RGMb is expressed on F4/80+CD11b+CD11cneg macrophages (RGMb+ macrophages), which accumulated in the lungs of OVA-sensitized and challenged mice, but not in naïve mice. Moreover, we found that a large fraction of the RGMb+ macrophages expressed the IL-25 receptor IL-17RB and produced IL-13. IL-25 was critical for the development of AHR in our model, since mice deficient in IL-17RB did not develop AHR. Finally, treatment with anti-RGMb mAb during the challenge phase of the protocol after allergen sensitization effectively prevented the development of AHR and airway inflammation, suggesting for the first time that RGMb+ cells, including RGMb+ macrophages, play critical roles in allergen-induced asthma. We used microarrays to compare the gene expression patterns in WT mice sensitized and challenged with OVA that were treated with either RGMb mAb or an isotype control. First replicate: 3 control samples (mice sensitized and challenged with saline), 3 RGMb mAb samples, 3 isotype samples; 2nd replicate: 3 control samples, 3 RGMb mAb samples, 2 isotype samples. Lung tissues were harvested at the same treatment time point in all groups.
2016-03-14 | E-GEOD-79156 | biostudies-arrayexpress
Project description:Metabolomics was used to identify metabolic fingerprints of AKT1 activation or MYC overexpression in human prostate tumors. Genomics was used to determine how many of these tumors had a genetic aberration underlying signaling activation. Copy number analysis of Affymetrix 250K SNP arrays was performed for 59 human prostate tumors and 6 normal prostate samples.
2014-10-20 | E-GEOD-62218 | biostudies-arrayexpress