Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene expression data in MDA231-LM2 breast cancer cells exposed to paclitaxel chemotherapy

ABSTRACT: In advanced malignancies, cancer cells have acquired capabilities to resist a variety of stress-inducing insults. We show that c-Jun N-terminal kinase (JNK) stress signaling is highly active in cancer cells from patients with late stage breast cancer and promotes tumor growth and metastasis in mouse models. Transcriptomic analysis revealed that JNK activity induces genes associated with extracellular matrix (ECM), wound healing and mammary stem cells. The ECM proteins and niche components osteopontin (SPP1) and tenascin C (TNC) are induced by JNK signaling and promote metastatic colonization of the lungs. Notably, treatment with chemotherapeutic drugs induces JNK activity in breast cancer cells, reinforcing the production of SPP1 and TNC. Inhibition of JNK or reduction of SPP1 or TNC expression sensitizes primary tumors and metastases in mice to chemotherapy. In order to investigate cancer cell-response to chemotherapy, we exposed MDA231-LM2 breast cancer cells to the chemotherapeutic agent paclitaxel and performed transcriptomic analysis using Affymetrix microarray.

ORGANISM(S): Homo sapiens

PROVIDER: GSE98238 | GEO | 2018/08/26

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Genes regulated by JNK signaling in MDA231-LM2 breast cancer cells

Project description:In advanced malignancies, cancer cells have acquired capabilities to resist a variety of stress-inducing insults. We show that c-Jun N-terminal kinase (JNK) stress signaling is highly active in cancer cells from patients with late stage breast cancer and promotes tumor growth and metastasis in mouse models. Transcriptomic analysis revealed that JNK activity induces genes associated with extracellular matrix (ECM), wound healing and mammary stem cells. The ECM proteins and niche components osteopontin (SPP1) and tenascin C (TNC) are induced by JNK signaling and promote metastatic colonization of the lungs. Notably, treatment with chemotherapeutic drugs induces JNK activity in breast cancer cells, reinforcing the production of SPP1 and TNC. Inhibition of JNK or reduction of SPP1 or TNC expression sensitizes primary tumors and metastases in mice to chemotherapy. We used Affymetrix microarrays to analyze the transcriptomic output modulated by JNK activity in a lung metastatic derivative of the MDA-MB-231 breast cancer cell line, MDA231-LM2.

2018-08-26 | GSE98237 | GEO

Gene expression data in MDA231-LM2 breast cancer cells cultured as oncospheres

Project description:In advanced malignancies, cancer cells have acquired capabilities to resist a variety of stress-inducing insults. We show that c-Jun N-terminal kinase (JNK) stress signaling is highly active in cancer cells from patients with late stage breast cancer and promotes tumor growth and metastasis in mouse models. Transcriptomic analysis revealed that JNK activity induces genes associated with extracellular matrix (ECM), wound healing and mammary stem cells. The ECM proteins and niche components osteopontin (SPP1) and tenascin C (TNC) are induced by JNK signaling and promote metastatic colonization of the lungs. Notably, treatment with chemotherapeutic drugs induces JNK activity in breast cancer cells, reinforcing the production of SPP1 and TNC. Inhibition of JNK or reduction of SPP1 or TNC expression sensitizes primary tumors and metastases in mice to chemotherapy. We used Affymetrix microarrays to investigate gene expression changes upon culturing metastatic breast cancer cells as oncospheres, in ultra-low adhesive plates in the absence of serum, in contrast to regular monolayer culture conditions.

2018-08-26 | GSE98239 | GEO

Long Noncoding RNA Expression profiling of IMP1-expression and IMP1 nonexpression MDA231 Cells

Project description:ZBP1/IMP1 is a RNA binding protein that post-transcriptionally regulates the expression of a handful mRNAs, implicated in maintaining cell polarity and adhesion. We have previously shown that ZBP1 was able to inhibit proliferation and invasiveness of breast carcinoma cells in vitro. To determine important LncRNA for breast tumor growth and metastasis in response to IMP1 expression, LncRNA expression data were obtained from, and compared between the breast cancer cell line MDA231-IMP1 and MDA231/GFP.

2016-12-09 | GSE91057 | GEO

Gene expression profiling of MDA231, BT549, and SUM159PT cells after selumetinib treatment or DUSP4 siRNA knockdown

Project description:MDA231, BT549, and SUM159PT basal-like breast cancer cell lines were transfected with non-targeting siRNA (siCONTROL), siRNA targeting DUSP4 (siDUSP4), or siCONTROL + 4 or 24 hr of 1uM selumetinib. Cells were harvested at 96 hr post-siRNA transfection. Data were Log2 RMA normalized. We sought to identify changes in gene expression after MEK inhibition, or after loss of DUSP4 function in breast cancer cell lines.

2013-09-03 | E-GEOD-41816 | biostudies-arrayexpress

Gene expression profiling of MDA231, BT549, and SUM159PT cells after selumetinib treatment or DUSP4 siRNA knockdown

2013-09-03 | GSE41816 | GEO

Identifcation of lncRNA MACC1-AS1-associated microRNAs in breast cancer cell line MDA231 using MS2-Tagged RNA Affinity Purification and miRNA-Seq

Project description:LncRNA MACC1-AS1 is the antisense RNA of MACC1 mRNA, which is located on the sixth intronic of MACC1 gene. MACC1-AS1 is an oncogenic lncRNA in colorectal cancer. But the function role of MACC1-AS1 in breast cancer is unknown. In the present study, We used MS2-Tagged RNA Affinity Purification and miRNA-Seq to characterize microRNAs that associated with MACC1-AS1 in breast cancer cell line MDA231.

2019-04-17 | GSE129873 | GEO

Gene expression profiling of MDA231 cells with alterations involving beta-oxidation pathway

Project description:In order to confirm the role of fatty acid Î²-oxidation in Src regulation, we performed gene expression analysis in MDA231 cells from in vivo model treated with ETX or knockdown of CPT1 or CPT2 using shRNA. As expected, inhibition of Î²-oxidation showed a gene expression pattern that is opposite to the published Src regulated gene pattern. The known Src up-regulated genes are down-regulated and Src down-regulated genes are up-regulated in Î²-oxidation inhibited cells. Western Blotting further confirmed the gene expression pattern. Knockdown of CPT1 or CPT2 inhibited Src Y416 autophosphorylation as observed with ETX. MDA231 cells were treated with ETX or knockdown of CPT1 or CPT2 using shRNA. Gene expression profiles were taken for each group and compared with control group (shRNA scramble). Multiple group comparison [MDA231-Scramble (C), MDA231-Scramble +ETX (D), MDA231-shCPT-1 (E) and MDA231-shCPT-2 (F)]

2016-04-14 | E-GEOD-72320 | biostudies-arrayexpress

Homo sapiens

Project description:Genes regulated by JNK signaling in MDA231-LM2 breast cancer cells

| PRJNA384365 | ENA

Characterization of Chemotherapy-treated PyMT Liver Matrisome

Project description:Metastasis accounts for 90% of cancer-related deaths, yet the mechanisms by which cancer cells colonize secondary organs remain poorly understood. For breast cancer patients, metastasis to the liver is associated with poor prognosis and a median survival of 6 months. Standard of care is chemotherapy, but recurrence occurs in 30% of patients. Systemic chemotherapy has been shown to induce hepatotoxicity and fibrosis, but how chemotherapy impacts the composition of the liver extracellular matrix (ECM) remains unknown. Individual ECM proteins drive tumor cell proliferation and invasion, features that are essential for metastatic outgrowth in the liver. Here, we characterize the liver ECM of tumor-bearing mice treated with and without chemotherapy using the MMTV-PyMT transgenic model of breast cancer. We identify distinct drug-specific changes induced by commonly used cytotoxic chemotherapies. We identify Collagen V as an ECM protein that is more abundant in livers isolated from paclitaxel-treated mice and identify mechanisms of Collagen V driven invasion via ECM organization and signaling through α1β1 integrins.

2022-10-05 | PXD036736 | Pride

Role of DNA methylation in FOXA1 cell type-specific recruitment to chromatin

Project description:CTCF, H2AFZ and FOXA1 genomic recruitment sites were determined using ChIP-chip while MeDIP-chip was used to monitor DNA methylation levels. Amplified and labeled DNA was hybridized to Affymetrix tiling arrays covering human chromosomes 8, 11 and 12. Cells used in this study are: MCF7 breast cancer cells, LNCaP prostate cancer cells, MDA-MB-231 breast cancer cells stably transfected with a FOXA1 expression vector (MDA231-FOXA1) or the empty control plasmid (MDA231-CTRL). H3K4me2 genomic distribution was determined using ChIP-chip. Amplified and labeled DNA was hybridized to Affymetrix tiling arrays covering human chromosomes 8, 11 and 12. Cells used in this study are MDA-MB-231 breast cancer cells stably transfected with a FOXA1 expression vector (MDA231-FOXA1) or the empty control plasmid (MDA231-CTRL).

2011-01-06 | GSE21513 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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