SOX2 and Tamoxifen Resistance
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Maria Vivanco
PROVIDER: E-MEXP-3984 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:We have completed the mouse expression microarray analysis of the 2 samples. Total RNA from each sample was quantified using the NanoDrop ND-1000 and the RNA integrity was assessed using standard denaturing agarose gel electrophoresis. For microarray analysis, Agilent Array platform was employed. The sample preparation and microarray hybridization were performed based on the manufacturerM-bM-^@M-^Ys standard protocols. Briefly, total RNA from each sample was amplified and transcribed into fluorescent cRNA with using the manufacturerM-bM-^@M-^Ys AgilentM-bM-^@M-^Ys Quick Amp Labeling protocol (version 5.7, Agilent Technologies). The labeled cRNAs were hybridized onto the Whole Mouse Genome Oligo Microarray (4x44K, Agilent Technologies). After having washed the slides, the arrays were scanned by the Agilent Scanner G2505C.Agilent Feature Extraction software (version 11.0.1.1) was used to analyze acquired array images. Quantile normalization and subsequent data processing were performed using the GeneSpring GX v11.5 software package (Agilent Technologies). After quantile normalization of the raw data, genes that at least 1 out of 2 samples have flags in Detected (M-bM-^@M-^\All Targets ValueM-bM-^@M-^]) were chosen for further data analysis. Differentially expressed genes between two samples were identified through fold change filtering. Pathway analysis and GO Analysis were applied to determine the roles of these differentially expressed genes played in these biological pathways or GO terms. Finally, Hierarchical Clustering was performed to show the distinguishable gene expression profiling between samples. beta cell lines (MIN6) were transfected with FTO vector or empty vector. The gene expression profiling of the two samples were performed by expression microarray analysis
2015-01-06 | E-GEOD-64668 | biostudies-arrayexpress
Project description:Kaposi sarcoma is the most common cancer in AIDS patients and is typified by red skin lesions. The disease is caused by the KSHV virus (HHV8) and is recognizable by its distinctive red skin lesions. The lesions are KSHV infected spindle cells, most commonly the lymphatic endothelial and blood vessel endothelial cells (LEC and BEC), plus surrounding stroma. Here we examine KSHVs modulation of Notch signaling using wild-type LEC cells co-cultured with DLL4 and JAG1 expressing LEC cells. Experiment Overall Design: There are 1) n=2 of LEC control cells co-cultured with pSIN expressing LEC, 2) n=3 of LEC co-cultured with pSIN-Dll4 expressing LEC, and 3) n=3 of LEC co-cultured with pSIN-JAG1 expressing LEC.
2009-12-05 | E-GEOD-16547 | biostudies-arrayexpress
Project description:mRNA expression profile modified by stable transfection of microRNA mir-517a (MIR517A) in a human hepatocellular carcinoma cell line Huh-7 Keywords: Hepatocellular carcinoma, Expression array, microRNA microRNA mir-517a (MIR517A) was transfected to Huh-7 cells using GFP-expressing lentiviral vector. Infected cells were selected using flow cytometry and subjected to mRNA expression microarray experiment. The profiles were compared to controls cells infected with only GFP protein.
2011-02-17 | E-GEOD-20679 | biostudies-arrayexpress
Project description:The dataset includes transcriptome profiling of U87-EGFRvIII cell lines with overexpression of human soluble LRIG1 (sLRIG1)
2019-12-01 | E-MTAB-7474 | biostudies-arrayexpress
Project description:Breast cancer cell lines containing the progesterone receptor respond to progestins, altering expression of a subset of genes. In a previously published experiment of inducible knock-down of histone H1 isoforms with an shRNA-expression lentivector (GSE12299), we modified the breast cancer cell line T47D with different vectors. Here, we explored response to progestin R5020 of control cells generated with the empty shRNA-expression vector. Stable breast cancer-derived cell lines containing the empty vector for inducible shRNA expression were grown for two days in the absence of serum. Progestin R5020 or vehicle was added for 6 hours, in duplicate, and RNA was extracted for microarray hybridization.
2013-10-14 | E-GEOD-25077 | biostudies-arrayexpress
Project description:Bladder cancer is one of the most common cancers. Since prognosis ameliorates with early detection, it is a challenge to develop techniques that could replace or complement the current diagnosis protocols. The study of extracellular vesicles (EVs) that are present in urine samples has become an attractive alternative. The present study describes the mRNA content of vesicles isolated from voided urine samples within bladder cancer context. To discover a genetic signature of cancer, RNA associated to EVs was analyzed by microarray technique. Total RNA isolated from Extracellular Vesicles obtained from urine of bladder cancer patients was compared with RNA isolated from urinary vesicles of non-cancer patients.
2014-01-29 | E-GEOD-51843 | biostudies-arrayexpress
Project description:This study aims to investigate differentially expressed proteins in tumor pericytes with or without TCAF2-ovexpression. Tumor pericytes were isolated from tumor of patients with colorectal cancer. Then, tumor pericytes were cultured, transfected with vector or TCAF2 overexpressing plasmid. Top ten cytokines were screened and Wnt5a was the most significant one.
2024-01-26 | PXD032935 | Pride
Project description:Elf5 (or ESE-2) is an ETS transcription factor that is abundantly expressed in the mammary epithelium, where it plays a critical role in dictating cell fate and lineage choices. These changes are in part mediated by alterations in the expression and activity of critical components of the Jak/Stat pathway. While the biological function of Elf5 in mammary gland development has been well characterized, its role in breast cancer remains to be elucidated. Here we show that loss of Elf5 leads to features associated with epithelial-mesenchymal transition (EMT) in the mouse mammary gland during pregnancy and lactation. These cellular changes in Elf5-null mammary epithelia are also reflected at the molecular level by the global enrichment of EMT-related gene signatures. ELF5 is expressed in higher level in weakly metastatic breast cancer cells that retained epithelial features compared to highly metastatic cells with mesenchymal features. ELF5 knockdown in T47D breast cancer cells resulted in EMT and increased migration. Conversely, ectopic expression of Elf5 revert mesenchymal-like MDA-MB-231 cells and its lung-tropic variant LM2 to an epithelial phenotype, with reduced migration, invasion and lung metastatic abilities. Finally, we showed that Elf5 binds directly to the promoter of the EMT transcriptional factor Snail2 (Slug) and repress its expression. Taken together, these data established a novel function for Elf5 in inhibiting EMT in normal mammary epithelium and in breast cancer through direct targeting of Snail2. This SuperSeries is composed of the following subset Series: GSE32143: LM2 cell: infected with lentivirus to stably express Elf5 vs GFP GSE32144: MDA-MB-231 cell: infected with lentivirus to stably express mut-Elf5 vs WT-Elf5
2012-09-20 | E-GEOD-32150 | biostudies-arrayexpress
Project description:Selective bromodomains inhibitors block the interaction between diverse bromodomains and extraterminal domains (BET) proteins and acetylated proteins. These inhibitors have shown beneficial effects in cancers malignancies and experimental inflammation in mouse models, but data on renal diseases are scarce. We have investigated the effect of the BET proteins inhibitor JQ1 in a mice model of unilateral ureteral obstruction. Treatment with JQ1 diminished renal damage, the presence of inflammatory cell infiltration and the upregulation of proinflammatory genes. The in vitro evaluation of JQ1 on TNF-α inducible genes in renal cells showed that BET inhibition modulated several biological processes, including inflammation or immune response. Moreover, gene-silencing experiments showed that BRD4 regulates several proinflammatory genes (IL-6, CCL-2 and CCL-5) and chromatin immunoprecipitation techniques demonstrated that BRD4 specifically binds to acetylated histone H3 in the promoter region of those genes. The nuclear factor-ï«B (NF-ï«B) pathway regulates renal inflammation. The RelA NF-ï«B subunit is activated by acetylation of lysine 310. In damaged kidneys and in TNF-α-treated renal cells, JQ1 blocked the nuclear translocation of RelA/NF-ï«B and NF-ï«B-mediated gene expression. Additionally, obstructed kidneys showed an activation of the Th17 immune response, which was diminished by JQ1 treatment. Our results demonstrate that the BET inhibition decreases renal inflammation by 3 independent mechanisms: 1) chromatin remodelling in the promoter regions of specific genes, 2) blocking NF-ï«B pathway activation, and 3) modulating the Th17 immune response. These results suggest that BET inhibitors could have important therapeutic applications in inflammatory renal diseases. HK2 cell line was treated with JQ1 or its enantiomer JQ1(-) (500nM) for 1 hour before stimulation or not with TNF-α (5ng/ml) for additional 3h. We analized the genes up- and down-regulated by TNF-α vs unstimulated cells, and further the genes downregulated or unaffected by JQ1 compared to the cells treated with the enantiomer (-) JQ1.
2016-07-01 | E-GEOD-71602 | biostudies-arrayexpress
Project description:To better understand the signaling complexity of AXL, a member of the TAM family of receptor tyrosine kinases, we created a physical and functional map of AXL signaling interactions, phosphorylation events, and target-engagement of three AXL tyrosine kinase inhibitors (TKI). We assessed AXL protein-complexes using BioID, effects of AXL TKI on global phosphoproteins using mass spectrometry, and target engagement of AXL TKI using activity-based protein profiling. BioID identifies AXL-interacting proteins that are mostly involved in cell adhesion/migration. Global phosphoproteomics reveal that AXL inhibition deregulates phosphorylation of peptides involved in phosphatidylinositol-mediated signaling and cell adhesion/migration. Comparison of three AXL inhibitors reveals that TKI RXDX-106 inhibits pAXL, pAKT and migration/invasion of these cells without reducing their viability, while Bemcentinib exerts AXL-independent phenotypic effects. Proteomic characterization of these TKIs reveals that they inhibit diverse targets in addition to AXL, with Bemcentinib having the most off-targets. AXL and EGFR TKI co-treatment did not reverse resistance in cell line models of Erlotinib resistance. However, a unique vulnerability was identified in one persister clone, wherein combination of Bemcentinib and Erlotinib inhibited cell viability and signaling. We also show that AXL is overexpressed in ~30-40% of NSCLC but rarely in SCLC. NSCLC cells have a wide range of AXL protein expression, with basal activation detected rarely. Overall, we evaluate the mechanisms of action of AXL in lung cancer which can be used to establish assays to measure drug targetable active AXL complexes in patient tissues and inform the strategy for targeting its signaling network as an anticancer therapy.
2022-10-14 | PXD023911 | Pride