Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Characteristics of Cross-Hybridization and Cross-Alignment in Pseudo-Xenograft samples by RNA-Seq and Microarrays [RNA-Seq]

ABSTRACT: In order to study molecular changes in the stroma from tissue samples it is recommended to separate tumor tissue from stromal tissue. This is particularly relevant to mouse tumor xenograft models where tumor, particularly metastatic tumors, can be small and difficult to separate from the host tissue. In our research we compared qualitatively the ability of high-throughput mRNA sequencing, RNA-Seq, and microarrays to detect tumor (human) and stromal (mouse) expression from mixed tumor-stromal samples in terms of the genes and pathways that are involved in cross-alignment (RNA-Seq) and cross-hybridization (microarrays). Human samples consisted of total RNA obtained from MDA-MB-231 human breast carcinoma cell line and isolated from three independent cultures of sub-confluent MDA-MB-231 cell lines in exponential phase of growth. Mouse samples were obtained from NOD scid gamma mice, and normal lung tissue was harvested from three independent age-matched mice.

ORGANISM(S): Mus musculus

SUBMITTER: Camilo Valdes

PROVIDER: E-GEOD-40890 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Simultaneous analysis of tumor and stromal gene expression profiles from xenograft models

Project description:Identifying the gene expression alterations that occur in both the tumor and stroma is essential to understanding tumor biology. We have developed a dual-species microarray analysis method that allows the dissection of both tumor and stromal gene expression profiles from xenograft models, based on limited interspecies cross-hybridization on Illumina gene expression beadchips. This methodology allows for simultaneous genome-wide analysis of gene expression profiles of both tumor cells and the associated stromal tissue. Data is provided regarding the crosshybridization of mouse liver RNA on human microarray, and MDA-MB-231 breast cancer cell line RNA on mouse microarray. Data is also provided for comparisons of MDA-MB-231 gene expression in vitro vs. in vivo, and mouse liver gene expression in control mice vs. stroma from MDA-MB-231 xenograft liver metastasis in tumor bearing mice A total of 18 samples were analyzed. Samples consist of 6 different types with each type in triplicate. Types are (1) MDA-MB-231 cell line grown in vitro and arrayed on mouse chips, (2) mouse liver from NOD/SCID mice arrayed on human chips, (3) MDA-MB-231 cell line grown in vitro arrayed on human chips, (4) MDA-MB-231 xenograft liver metastasis arrayed on human chips, (5) mouse liver from NOD/SCID mice arrayed on mouse chips, and (6) MDA-MB-231 xenograft liver metastasis arrayed on mouse chips. The overall design had three objectives: (1) to determine crosshybridizing probes based on sample types 1, 2, 3, and 5, (2) detect stromal and tumor expression using sample types 4 and 6, and (3) determine genes differentially expressed in tumor or metastasis compared to normal by comparing sample types 3 and 4 and comparing sample types 1 and 5.

2011-11-22 | E-GEOD-30993 | biostudies-arrayexpress

Oct4 affects E-cadherin expression via regulating Rnd1 associated cytoskeleton rearrangement in breast cancer cells

Project description:Oct4, a key transcription factor for maintaining the pluripotency and self-renewal of stem cells has been reported previously. It also plays an important role in tumor proliferation and apoptosis, but the role of Oct4 been in tumor metastasis is still not very clear. Here, we found that ectopic expression of Oct4 in breast cancer cells can inhibit their migration and invasion. Detailed examinations revealed that Oct4 up-regulates expression of E-cadherin, indicative of its inhibitory role in epithelial-mesenchymal transition (EMT). RNA-sequence assay showed that Oct4 down-regulates expression of Rnd1. As an atypical Rho protein, Rnd1 can affect cytoskeleton rearrangement and regulate cadherin-based cell-cell adhesion by antagonizing the typical Rho protein, RhoA. Ectopic expression of Rnd1 in MDA-MB-231 cells changes cell morphology which influences cell adhesion and increases migration. It is reported that EMT is accompanied by cytoskeleton remodeling, we hypothesized that Rnd1 may play a role in regulating EMT. Over-expression of Rnd1 can partly rescue the inhibitory effects induced by Oct4, not only migration and invasion, but also in E-cadherin level and cellular morphology. Furthermore, silencing of Rnd1 can up-regulate the expression of E-cadherin in MDA-MB-231 cells. These results present evidence that ectopic expression of Oct4 increases E-cadherin and inhibits metastasis, effects which may be related to Rnd1 associated cell-cell adhesion in breast cancer cells. Examination of mRNA profiles in MDA-MB-231 cells with OCT4 overexpressing

2014-01-25 | E-GEOD-54392 | biostudies-arrayexpress

26S proteasome is conserved, therapeutically relevant mediator of mutant p53 gain-of-function in cancer

Project description:Mutant p53 proteins, resulting form frequent TP53 tumor suppressor missense mutations, possess gain-of-function activities and are among the most widespread and robust oncoproteins in human tumors. They are potentially important but understudied therapeutic targets. No studies to date have distinguished common, therapeutically relevant mutant p53 gain-of-function effects, from effects specific to different mutant variants and cell backgrounds. Here we identify 26S proteasome machinery as the common downstream effector controlled by mutant p53s in Triple Negative Breast Cancer (TNBC - aggressive carcinomas with TP53 as the most frequently mutated locus) and conserved in other human cancers. We have identified this pathway using a combination of single-model, multi-method vertical analysis (whole cell proteome, RNA sequencing an ChIP sequencing) and multi-cell line, horizontal analysis of transcriptiomes. We found that different missense mutant p53s regardless of the cell background transcriptionaly activate whole 26S proteasome machinery. Proteasome activity is significantly increased in p53 mutant versus wild-type or knockdown/null status - in cellular and mouse models as well as in human breast tumors. Increased proteasome activity leads to inhibition of tumor suppressive pathways. The control of mutant p53 over proteasome transcription and activity results in the increased resistance to proteasome inhibitors. By combining the mutant p53 targeting agents and proteasome inhibitor we were able to overcome the “bounce-back” proteasome inhibitor resistance mechanism in mutant p53 bearing TNBC cells and xenografts in vivo.

2016-05-03 | PXD001673 | Pride

Small RNAseq of human breast cancer cell line MDA-MB-231 transfected with antisense oligonucleotide 1537S (ASO-1537S), compared to control oligonucleotide (ASO-C) and untreated cells

Project description:Proliferation of tumor cells transfected with ASO-1537S is inhibited compared to controls. The aim of the experiment is to determine changes in microRNA expression profiles with treatment, compared to controls, using 3 biological replicates for each condicition.

2023-06-02 | E-MTAB-6768 | biostudies-arrayexpress

Preliminary small RNAseq of human breast cancer cell line MDA-MB-231 transfected with antisense oligonucleotide 1537S (ASO-1537S), compared to control oligonucleotide (ASO-C) and untreated cells

2023-06-02 | E-MTAB-6762 | biostudies-arrayexpress

MDA-MB-231/1833 bone-metastatic breast cancer cell gene expression after conditioning in conditioned medium from HUVECs conditioned in conditioned medium from static and flow-stimulated MLO-Y4 osteocytes

Project description:Bone metastases is a common severe complication for breast cancer. We previously showed that conditioned medium (CM) from osteocytes stimulated with oscillatory fluid flow, mimicking bone mechanical loading during routine physical activities, reduced breast cancer cell extravasation across endothelial monolayers. Endothelial cells are situated at an ideal location to mediate signals between osteocytes in the bone matrix and metastasizing cancer cells in the blood vessels. Therefore, we used RNA sequencing to show that CM from endothelial cells conditioned in CM from flow-stimulated osteocytes significantly altered gene expression in bone-metastatic breast cancer cells. This This provides insights into the capability of bone-loading activity in preventing bone metastases.

2018-11-13 | E-MTAB-7176 | biostudies-arrayexpress

Quantitative phosphoproteomic analysis reveals reciprocal activation of receptor tyrosine kinases between cancer epithelial cells and their interacting stromal fibroblast cells

Project description:Communication and interaction between carcinoma associated fibroblast (CAF) cells and tumor epithelium cells plays a critical role in cancer initiation and progression. However, a mechanistic understanding of how CAFs communicate with tumor cells to promote their proliferation and invasion is far from complete. In this study, we employed a SILAC labeling based co-culture system coupled with mass spectrometry analysis to identify and quantify the early phospho-signaling transductions induced by the crosstalk between CAFs and tumor cells. We performed three-state SILAC labeling for MDA-MB-231 and 82T. 9 million light labeled 82-L cells were co-cultured with medium labeled MDA-MB-231-M cells for 30 minutes. 9 million heavy labeled 82T-H cells were individually cultured in heavy SILAC media with for 30 minutes. Both individually cultured and co-cultured cells were quickly harvested with 9 M urea lysis buffer and mixed together. Mixed lysates were sonicated, reduced, alkylated and digested by trypsin. Tryptic peptides were desalted using SepPak C18 cartridge and followed by phosphotyrosine peptide enrichment using immunoaffinity purification with pY100 antibody. The enriched phosphopeptides were analyzed using a reverse-phase liquid chromatography system interfaced with an LTQ-Orbitrap Velos mass spectrometer. The Proteome Discoverer (v2.0; Thermo Fisher Scientific) suite was used for quantitation and database searches. The tandem mass spectrometry data were searched using SEQUEST search algorithm against a Human RefSeq database supplemented with frequently observed contaminants. The probability of phosphorylation sites was determined from the PhosphoRS algorithm.

2018-10-26 | PXD003544 | Pride

Ligand-dependent genomic function of glucocorticoid receptor in triple-negative breast cancer

Project description:Glucocorticoids (GC) have been widely used as coadjuvants in the treatment of solid tumors, but GC treatment may be associated with poor pharmacotherapeutic response and/or prognosis. The genomic action of GC in these tumors is largely unknown. Here we find that dexamethasone (Dex, a synthetic GC) regulated genes in triple-negative breast cancer (TNBC) cells are associated with drug resistance. Importantly, these GC-regulated genes are aberrantly expressed in TNBC patients and associated with unfavorable clinical outcomes. Interestingly, in TNBC cells, Compound A (CpdA, a selective GR modulator) only regulates a small number of genes not involved in carcinogenesis and therapy resistance. Mechanistic studies using a ChIP-exo approach reveal that Dex- but not CpdA-liganded glucocorticoid receptor (GR) binds to a single glucocorticoid response element (GRE), which drives the expression of pro-tumorigenic genes. Our data suggest that development of safe coadjuvant therapy should consider the distinct genomic function between Dex- and CpdA-liganded GR. To study GR-regulated genes and define GRE in human genome, RNA-seq and GR ChIP-exo are performed in MDA-MB-231 cells before/after dex and CpdA stimulation. Each experiment includes two replicates.

2015-09-18 | E-GEOD-56022 | biostudies-arrayexpress

Uncoupling effects of ERalfa on LKB1/AMPK interaction upon adiponectin exposure in breast cancer

Project description:Adipose tissue is a metabolic and endocrine organ that secretes numerous bioactive molecules called adipocytokines. Among these, adiponectin has been argued to have a crucial role in obesity-associated breast cancer. The key molecule of adiponectin signaling is AMP-activated protein kinase (AMPK), mainly activated by Liver Kinase B1 (LKB1). Here, we demonstrated how the ERalfa/LKB1 interaction may negatively interfere with the capability of LKB1 to phosphorylate AMPK and then inhibit its downstream signaling TSC2/mTOR/p70S6k. In MCF-7 cells upon adiponectin AMPK signaling was not working, keeping its downstream protein Acetyl-CoA Carboxylase (ACC) still active. In contrast, in MDA-MB-231 cells the phosphorylation of AMPK and ACC was enhanced with consequent inhibition of both lipogenesis and cell growth. Thus, upon adiponectin, ERalfa signaling switched the energy balance of breast cancer cells towards a lipogenic phenotype. In other words, adiponectin in all the concentrations tested played an inhibitory role on ERalpha-negative breast cancer cell growth and progression either in vitro or in vivo. In contrast, low adiponectin levels, similar to those circulating in obese patients, worked on ERalfa-positive cells as a growth factor, stimulating their growth and progression. The latter effect seems to be blunted in vivo only in the presence of high adiponectin concentration. Based on the present results, it can be concluded that if we prospectively address adiponectin as a pharmacological tool, a separate therapeutic treatment should be carefully assessed in ERalfa-positive and negative breast-cancer patients.

2020-02-27 | E-MTAB-6120 | biostudies-arrayexpress

GATA3 Reprograms Basal Breast Cancer Cells towards a Luminal Subtype and Inhibits Metastases through Suppression of Lysyl Oxidase

Project description:The transcription factor GATA3 is essential for luminal cell differentiation during mammary gland development and critical for formation of the luminal subtypes of breast cancer. Ectopic expression of GATA3 promoted global alterations of the transcriptome of basal triple-negative breast cancer cells resulting in molecular and cellular changes associated with a more differentiated, luminal tumor subtype and a concomitant reduction in primary tumor growth, lung metastasis, and macrophage recruitment at the metastatic site. Importantly, we demonstrate that the inhibition of metastases by GATA3 results from the suppression of lysyl oxidase (LOX) expression, a metastasis promoting matrix protein that affects cell proliferation, cross-linking of extracellular collagen types, and establishment of the metastatic niche. There are 2 samples sent in triplicates.

2011-08-31 | E-GEOD-24249 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data