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

Gene expression signatures for breast cancer cells metastatic to bone marrow

ABSTRACT: To clarify and compare gene expression profile of each cell line, we have employed microarray expression profiling. The expression of many genes was similar in MM231-D3H2LN-GFP-BM2 cells parental cells, MM231-D3H2LN-GFP cells; however, the expression of genes related to the cell cycle was decreased in the BM2 cells compared with the parental cells. We also confirmed that the global gene expression patterns of the CD44+ and CD44- MM231-D3H2LN-GFP-BM2 cells were similar, although some genes which encode proteins that breast cancer cell dormancy, such as SRC and ERBB2 were increased and decreased, respectively, in the CD44- population. The gene expression of breast cancer cells metastatic to bone marrow and those with or without expression of cancer stem cell marker were measured.

ORGANISM(S): Homo sapiens

SUBMITTER: Yusuke Yoshioka

PROVIDER: E-GEOD-57921 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

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

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

Transcription profiling of Pseudomonas aeruginosa strain PA01 grown in swimming of swarming conditions

Project description:Microarray were done on 4 independent cultures. PA01 was grown for 6 hours to late log growth phase (OD600 0.9-1.0) in liquid BM2-swarming media under shaking conditions(swimming) or for 18 hours at 37C on BM2-swarming plate containing 0.5% (w/v) agar and 0.1% casamino acids. Cells were harvested either by centrifugation(swimming) or by a sterile inoculating loop (swarming) and were resuspended n BM2-swarming media supplement with RNAprotect reagent (Qiagen)

2008-03-01 | E-FPMI-10 | biostudies-arrayexpress

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

Isolation and characterization of a metastatic hybrid cell line generated by ER negative and ER positive breast cancer cells in mouse bone marrow

Project description:The origin and the contribution of breast tumor heterogeneity to its progression are not clear. We investigated the effect of a growing orthotopic tumor formed by an aggressive estrogen receptor (ER)-negative breast cancer cell line on the metastatic potential of a less aggressive ER-positive breast cancer cell line for the elucidation of how the presence of heterogeneous cancer cells might affect each other’s metastatic behavior. ER positive ZR-75-1/GFP/puro cells, resistant to puromycin and non-tumorigenic/non-metastatic without exogenous estrogen supplementation, were injected intracardiacally into mice bearing growing orthotopic tumors, formed by ER negative MDA-MB-231/GFP/Neo cells resistant to G418. A variant cell line B6, containing both estrogen-dependent and -independent cells, were isolated from GFP expressing cells in the bone marrow and re-inoculated in nude mice to generate an estrogen-independent cell line B6TC.

2011-05-25 | E-GEOD-27515 | biostudies-arrayexpress

DNA microarray studies of tumors grown in nude mice from breast cancer cells MDA-MB-231 overexpressing or not the angiotensin II AT2 receptor, and treated or not with AT2 agonist compound C21

Project description:This experiment aims at investigating the effect of AT2 overexpression and/or activation in breast cancer. Human breast cancer cells MDA-MB-231 were transfected with lentiviral construct containing flagged human AT2 receptor sequence (or empty vector) and were subcutaneously injected into immuno-deficient mice (2. 10e6 cells). When the tumors reached 5 mm3 volume, mice were treated daily with compound C21 (0.3 mg/kg) or vehicle for 43 days. Total RNA was extracted from tumors and submitted to DNA array analysis.

2020-11-07 | E-MTAB-8532 | biostudies-arrayexpress

Expression data of control-shRNA and SATB1-shRNA expressing MDA-MB-231 cells from 2D and 3D culture system

Project description:We examined whether SATB1 functions as a global gene regulator in order to maintain the aggressive phenotype of the MDA-MB-231 cell line. We compared the gene expression profiles between control_shRNA-MDA-MB-231 cells, which express SATB1 at high levels, and SATB1_shRNA1-MDA-MB-231 in which the level of SATB1 was greatly downregulated by RNAi technology. This comparative studies were performed using two different platforms (Codelink and Affymetrix genechip) with two culture conditions either on plastic dish (2D) or on matrigel (3D) which allows cells to form a breast-like morphology only for non-aggressive cells. Keywords: Comparative studies on Control_shRNA and SATB1_shRNA1 expressing MDA-MB-231 from 2D or 3D culture. We examined control_shRNA-MDA-MB-231 cells and SATB1_shRNA1-MDA-MB-231 cells under two culture condition;on plastic dish(2D culture) and on Matrigel coated dish(3D culture). When SATB1 was depleted by RNAi technology, these normally aggressive cells exhibited normal breast like morphology on 3D. We used two different microarray platforms (Codelink and Affymetrix) to make expression data. Initial analysis of data and cross-platform comparison were performed using Codelink expression analysis and GeneSpring software. We provide ratio for control_shRNA/SATB1_shRNA1-MDA-MB-231 cells for 2D and 3D on this series.

2010-05-26 | E-GEOD-5417 | 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

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

Paclitaxel resistant MDA-MB-231 Cells and resensitization with bexarotene treatment

Project description:Acquired drug resistance represents a major challenge in chemo-therapy treatment for various types of cancers. We have found that the retinoid X receptorâselective agonist bexarotene (LGD1069, Targretin) was efficacious in treating chemo-resistant cancer cells. The goal of this microarray study was to understand the mechanism of bexaroteneâs role in overcoming acquired drug resistance using human breast cancer cells MDA-MB-231 as a model system and paclitaxel as model compound. After MDA-MB-231 cells were repeatedly treated with paclitaxel for 8 cycles with each cycle including a 3-day treatment with 30 nM paclitaxel and followed by a 7-day exposure to control medium, MDA cells resistant to paclitaxel were developed and their growth was no longer inhibited by paclitaxel treatment. Those MDA cells with acquired drug resistance, when treated with paclitaxel and bexarotene in combination, could regain their sensitivity and their growth were again inhibited. Therefore, RNA samples from parental MDA-MB-231 cells, paclitaxel-resistant MDA cells treated with vehicle, paclitaxel alone or in combination with bexarotene, were used for perform global gene expression profiling with Affymetrix HG-U133A gene chips. Keywords: Drug Treatment MDA-MB-231 cells were exposed to regimens on a 10-day cycle: a 3-day treatment with 30 nM paclitaxel and followed by a 7-day exposure to control medium. Paclitaxel resistant MDA-MB-231 cells (MDA-PR) were established within 8 cycles of such treatment (80 days). These MDA-PR cells were then treated with vehicle control, paclitaxel along, or the combination of 30 nM paclitaxel ( 3 days on and 7 days off) and 1 ÂµM Targretin (10 days on) in a new 10-day cycle for 3 months. Thus, there are four treatment groups, parent MDA cells, MDA-PR, MDA-PR treated with paclitaxel, MDA-PR treated with paclitaxel and bexarotene, and each group had four biological replicates.

2011-07-18 | E-GEOD-12791 | 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