Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Genome-wide analysis of gene expression in MDA-MB-231 breast cancer cells in response to conditional miRNA mediated BSP knockdown

ABSTRACT: Our goal was to identify the genes, which are modulated following conditional BSP knockdown for 3 and 6 days. Thus, to elucidate the BSP relevance and to broaden the knowledge on the affected signalling pathways. Cell pellets were collected after 3 and 6 days of cultivating the cells in media with or without doxycycline. There were duplicated total RNA samples for each time interval and each condition.The mRNA expression of the in vitro miRNA treated cells was compared to the respective +dox control.

ORGANISM(S): Homo sapiens

SUBMITTER: Berger Martin

PROVIDER: S-ECPF-GEOD-55432 | biostudies-other |

REPOSITORIES: biostudies-other

ACCESS DATA

Json Xml

Similar Datasets

Genome-wide analysis of gene expression in MDA-MB-231 breast cancer cells in response to conditional miRNA mediated BSP knockdown.

2014-02-28 | GSE55432 | GEO

Genome-wide analysis of gene expression in MDA-MB-231 breast cancer cells in response to conditional miRNA mediated BSP knockdown.

Project description:Our goal was to identify the genes, which are modulated following conditional BSP knockdown for 3 and 6 days. Thus, to elucidate the BSP relevance and to broaden the knowledge on the affected signalling pathways. Cell pellets were collected after 3 and 6 days of cultivating the cells in media with or without doxycycline. There were duplicated total RNA samples for each time interval and each condition.The mRNA expression of the in vitro miRNA treated cells was compared to the respective +dox control.

2014-02-28 | E-GEOD-55432 | biostudies-arrayexpress

Hypoxic MDA-MB-231 miRNA array

Project description:MiR-544 was inhibited by either a miR-544 antagomir or compound 1 under hypoxic conditions in MDA-MB-231 cells MiRNA microarray was utilized to examine the specificity of 1 for miR-544. 3 MDA-MB-231 samples treated with a miR-544 antagomir or compound 1 were subjected to hypoxia for a period of 5 days. After 5 days, samples were pooled and subjected to miRNA microarray analysis.

| S-ECPF-GEOD-64436 | biostudies-other

Genome-wide analysis of gene expression in MDA-MB-231 breast cancer cells in response to conditional miRNA mediated OPN knockdown

Project description:Our goal was to identify the genes, which are modulated following conditional OPN knockdown for 3 and 6 days. Thus, to elucidate the OPN relevance and to broaden the knowledge on the affected signalling pathways.

2019-11-04 | GSE133608 | GEO

The miRNA profiling in MDA-MB-231, MDA-MB-231/E1A and knockdown of Dicer in MDA-MB-231/E1A cells

Project description:Dicer, RNase III endonuclease, is an essential enzyme in miRNA biogenesis that regulates target gene expression, and it has been reported that aberrant expressions of Dicer associate with the clinical outcomes of patients in various cancers. To explore the miRNA differencial expression regulated by Dicer in MDA-MB-231/E1A cells, the microarray profiling analysis was employed to conduct differentially expressed miRNAs in stable MDA-MB-231/vector, MDA-MB-231/E1A, and MDA-MB-231/E1A/shDicer cells.

2016-01-16 | GSE76924 | GEO

The miRNA profiling in MDA-MB-231, MDA-MB-231/E1A and knockdown of Dicer in MDA-MB-231/E1A cells

2016-01-16 | E-GEOD-76924 | biostudies-arrayexpress

Impaired G2/M cell cycle arrest induces apoptosis in pyruvate carboxylase knockdown MDA-MB-231 cells.

Project description:BackgroundPrevious studies showed that suppression of pyruvate carboxylase (PC) expression in highly invasive breast cancer cell line, MDA-MB-231 inhibits cell growth as a consequence of the impaired cellular biosynthesis. However, the precise cellular mechanism underlying this growth restriction is unknown.MethodsWe generated the PC knockdown (PCKD) MDA-MB-231 cells and assessed their phenotypic changes by fluorescence microscopy, proliferation, apoptotic, cell cycle assays and proteomics.ResultsPC knockdown MDA-MB-231 cells had a low percentage of cell viability in association with accumulation of abnormal cells with large or multi-nuclei. Flow cytometric analysis of annexin V-7-AAD positive cells showed that depletion of PC expression triggers apoptosis with the highest rate at day 4. The increased rate of apoptosis is consistent with increased cleavage of procaspase 3 and poly (ADP-Ribose) polymerase. Cell cycle analysis showed that the apoptotic cell death was associated with G2/M arrest, in parallel with marked reduction of cyclin B levels. Proteomic analysis of PCKD cells identified 9 proteins whose expression changes were correlated with the degree of apoptosis and G2/M cell cycle arrest in the PCKD cells. STITCH analysis indicated 3 of 9 candidate proteins, CCT3, CABIN1 and HECTD3, that form interactions with apoptotic and cell cycle signaling networks linking to PC via MgATP.ConclusionsSuppression of PC in MDA-MB-231 cells induces G2/M arrest, leading to apoptosis. Proteomic analysis supports the potential involvement of PC expression in the aberrant cell cycle and apoptosis, and identifies candidate proteins responsible for the PC-mediated cell cycle arrest and apoptosis in breast cancer cells.General significanceOur results highlight the possibility of the use of PC as an anti-cancer drug target.

| S-EPMC7806519 | biostudies-literature

Knockdown of PTOV1 and PIN1 exhibit common phenotypic anti-cancer effects in MDA-MB-231 cells.

Project description:BackgroundEarlier, we have identified PTOV1 as a novel interactome of PIN1 in PC-3 cells. This study aims to explore the functional similarity and the common role of both genes in breast cancer cell proliferation.MethodsCTG, crystal violet assay, clonogenic assay, wound healing assay, cell cycle analysis, Hoechst staining and ROS measurement were performed to assess cell viability, colony forming potential, cell cycle arrest, nuclear condensation and ROS production after knocking down of PTOV1 and PIN1 by siRNAs in MDA-MB-231 and MCF-7 cells. CO-IP, qPCR and western blot were performedto study interaction, transcriptional and translational regulation of both genes.ResultsKnockdown of PTOV1 and PIN1 inhibited the cell proliferation, colony formation, migration, cell cycle, and induced nuclear condensation as well as ROS production. Interaction of PTOV1 and PIN1 was validated by Co-IP in MDA-MB-231 cells. Genes involved in cell proliferation, migration, cell cycle, and apoptosis were regulated by PIN1 and PTOV1. PTOV1 knockdown inhibited Bcl-2, Bcl-xL and inducedBAX, LC3 and Beclin-1expression. Overexpression of PIN1 increased the expression of PTOV1. Knockdown of both genes inhibited the expression of cyclin D1, c-Myc, and β-catenin.ConclusionsPTOV1 and PIN1 interact and exert oncogenic role in MDA-MB-231 cells by sharing the similar expression profile at transcriptional and translational level which can be a promising hub for therapeutic target.

| S-EPMC6513092 | biostudies-literature

Expression data from CD44-knockdown MDA-MB-231 human breast cancer cells

Project description:CD44, an adhesion molecule that binds to extracellular matrix, primarily to hyaluronan (HA), has been implicated in cancer cell migration, invasion, and metastasis. CD44 has also recently been recognized as a marker for stem cells of several types of cancer. However, the roles of CD44 in the development of bone metastasis still remain unclear. To explore this issue, we established the MDA-MB-231 human breast cancer cells stably expressing short hairpin RNA against CD44. The CD44-knockdown MDA-MB-231 cells (MDA-MB-231 shCD44-2 and shCD44-3) were analyzed. As control, MDA-MB-231 cells stably expressing shRNA against firefly luciferase (shLuc) were used. Total of three samples. No replicates.

| S-ECPF-GEOD-45613 | biostudies-other

Long noncoding RNA and mRNA profiling in MDA-MB-231 cells following RNAi-mediated knockdown of SIRT7.

Project description:Breast cancer is one of the most common malignant cancers among women and a major clinical obstacle. Although studies have reported the abnormal expression of SIRT7 in breast cancer, whether the function of SIRT7 regulates the expression of long noncoding RNAs (lncRNAs) in breast cancer remains unknown. We aimed to determine the differential expressions of mRNAs and lncRNAs associated with SIRT7 and understand the regulatory mechanism of SIRT7 in breast cancer. RNA sequencing was performed to explore the transcriptome in MDA-MB-231 cells after SIRT7 depletion, and a total of 50,634 different transcripts were identified. In comparison with the negative control, siSIRT7 groups showed 240 differentially expressed mRNAs and 26 differentially expressed lncRNAs. Gene ontology analysis revealed that the differentially expressed mRNAs mainly regulated DNA replication, CXCR chemokine receptor binding, and maturation of large subunit rRNA from tricistronic rRNA transcript, nucleoplasm, mitochondrion, and NAD+ ADP-ribosyltransferase activity. Kyoto Encyclopedia of Genes and Genomes analysis showed that the differentially expressed mRNAs were mainly involved in pathways associated with MAPK signaling pathway, tumor necrosis factor signaling pathway, hepatitis B, and cancer. Moreover, the target genes of the differentially expressed lncRNAs mainly regulated the carboxylic acid metabolic processes and were involved in glycolysis pathway. The mRNA-lncRNA coexpression network comprised 186 mRNAs and 23 lncRNAs. Our results provide essential data regarding differentially expressed lncRNAs and mRNAs after the depletion of SIRT7 in breast cancer cells, which may be useful to elucidate the role of SIRT7 in breast cancer development.

| S-EPMC5661475 | biostudies-literature

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