Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

E-GEOD-12791

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

OTHER RELATED OMICS DATASETS IN: PRJNA112787

PROVIDER: E-GEOD-12791 | ExpressionAtlas | 2015-08-06

REPOSITORIES: ExpressionAtlas

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	E-GEOD-12791-analysis-methods.tsv	Tabular
	E-GEOD-12791-atlasExperimentSummary.Rdata	Rdata
	E-GEOD-12791-configuration.xml	Xml
	E-GEOD-12791-percentile-ranks.tsv	Tabular
	E-GEOD-12791.condensed-sdrf.tsv	Tabular

Items per page:

1 - 5 of 98

Similar Datasets

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

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

2011-07-19 | GSE12791 | GEO

Expression data from MDA-MB-231 parental and xenograft tumor cells treated with Smac mimetic SM-164.

Project description:Small-molecule Smac mimetics target inhibitor of apoptosis (IAP) proteins to induce TNFÎ±-dependent apoptosis in cancer cells and several Smac mimetics have been advanced into clinical development as a new class of anticancer drugs. However, preclinical studies have shown that only a small subset of cancer cell lines are sensitive to Smac mimetics used as single agents and these cell lines are at risk of developing drug resistance to Smac mimetics. Thus, it is important to understand the molecular mechanisms underlying intrinsic and acquired resistance of cancer cells to Smac mimetics in order to develop effective therapeutic strategies to overcome or prevent Smac mimetic resistance. We established Smac mimetic resistant sublines derived from MDA-MB-231 breast cancer cells, which exhibit exquisite sensitivity to the Smac mimetic SM-164, and used microarrays to detail the global programme of gene expression underlying SM-164 resistance in MDA-MB-231 cells and identified differentially expressed genes in SM-164-resistant and -sensitive MDA-MB-231 cells. SCID mice with MDA-MB-231 xenograft tumors were treated with 5 mg/kg of SM-164 intravenously for 5 days/week for 2 weeks. SM-164-regressed MDA-MB-231 tumors regrew after treatment ended. Tumor cells from these regrown MDA-MB-231 tumors were isolated and total RNAs were prepared for microarray analysis.

2012-03-01 | E-GEOD-33827 | biostudies-arrayexpress

ATAC-seq in cadmium resistant breast cancer MDA-MB-231 cells

Project description:In this study, we compared ATAC-seq of cadmium resistant MDA-MB-231 cells vs untreated controls.

2023-02-20 | GSE216496 | GEO

Induction of CTH expression in response to amino acid starvation confers resistance to anti-LAT1 therapy in MDA-MB-231 cells

Project description:We examined gene expression change under amino acid restriction in JPH203 treated MDA-MB-231 and T-47D cells. JPH203 treatment induced endoplasmic reticulum stress response via amino acid starvation stress pathway in both MDA-MB-231 and T-47D cells. Moreover, MDA-MB-231 was upregulated anti-oxidants related genes.

2022-01-26 | GSE173698 | GEO

MiRNA-based on genome-wide maps in MDA-MB-231 cells treated with or without Tanshinone IIA (TSA).

Project description:Analysis of MDA-MB-231 cells following TSA treatment or not. TSA regulates various miRNA expression in MDA-MB-231 cells.Results provide insight into the role of miRNAs-involved mechanisms underlying TSA-mediated effects on breast cancer stemness.

2022-01-01 | GSE156155 | GEO

CUT&RUN in cadmium resistant breast cancer MDA-MB-231 cells

Project description:In this study, we compared MTF-1 CUT&RUN of cadmium resistant MDA-MB-231 cells vs untreated controls.

2023-02-20 | GSE222587 | GEO

Gene expression profile in breast cancer cells

Project description:We report the gene expression patterns in MDA-MB-231 (a line selected for low metastatic ability), MDA-MB-231-1833 (its bone-tropic metastatic derivative line), MDA-MB-231p27CK-DD (a phosphomimetic cell line), MDA-MB-231-1833shp27 (p27 knockdown cell line), MDA-MB-231-1833PF1502 (PI3K inhibitor treatment). It shows that the gene expression pattern are regulated in a p27 phosphorylation-dependent manner.

2019-03-19 | GSE112445 | GEO

LncRNA Uc003xsl.1 Activates of NF-κB/IL8 Axis to Promotes Triple-negative Breast Cancer Progression via A Decoy Role to NKRF [lnc231]

Project description:To discover the potential drivers of TNBC metastasis, we established an in vivo model by injecting MDA-MB-231cells into the tail veins of mice. Then, the breast tumor cells that successfully grew into metastatic lung tumors were collected and expanded in vitro, followed by re-injected into the tail veins of mice for lung metastasis. After three rounds of selection, a highly metastatic subline, MDA-MB-231-P3, was established, and more frequent micro-metastasis was detected in MDA-MB-231-P3 groups than that of MDA-MB-231 groups when the lungs of mice were stained with hematoxylin and eosin (HE). The lncRNA profiles of MDA-MB-231 or MDA-MB-231-P3 cells were analyzed by lncRNA sequencing. A total of 267 lncRNAs in MDA-MB-231-P3 cells were upregulated more than 2-fold in comparison to the MDA-MB-231 cells.

2021-11-29 | GSE163900 | GEO

Tang2019 - Pharmacology modelling of AURKB and ZAK interaction in TNBC

Project description:Aurora Kinase B and ZAK interaction model Equivalent of the stochastic model used in "Network pharmacology model predicts combined Aurora B and ZAK inhibition in MDA-MB-231 breast cancer cells" by Tang et. al. 2018. The only difference is cell division and partitioning of the components, which are available in the original model for SGNS2.

2024-09-02 | BIOMD0000000940 | BioModels

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