Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

14 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Examination of the role of peptidylarginine deiminase 2 (PAD2) in gene expression in MCF-7 breast cancer cells

ABSTRACT: To investigate the potential role of peptidylarginine deiminase 2 (PAD2) in gene expression, we created stable shRNA scrambled control and PAD2 knockdown MCF-7 breast cancer cell lines. After validating the specific knockdown of PAD2 at the mRNA and protein level, we utilized an Agilent microarray platform to compare the gene expression profile of the two cell lines to generate a candidate list of genes regulated by PAD2. Control and PAD2 knockdown cells were created by stably transfecting shRNA constructs into MCF-7 cells. Stable cells were selected using puromycin and knockdown validate at the mRNA and protein level. Microarray data represents 4 independent biological replicates contain control and PAD2 knockdown samples.

ORGANISM(S): Homo sapiens

SUBMITTER: Scott Coonrod

PROVIDER: E-GEOD-37087 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Examination of the role of peptidylarginine deiminase 2 (PAD2) in gene expression in MCF-7 breast cancer cells

Project description:To investigate the potential role of peptidylarginine deiminase 2 (PAD2) in gene expression, we created stable shRNA scrambled control and PAD2 knockdown MCF-7 breast cancer cell lines. After validating the specific knockdown of PAD2 at the mRNA and protein level, we utilized an Agilent microarray platform to compare the gene expression profile of the two cell lines to generate a candidate list of genes regulated by PAD2.

2012-04-07 | GSE37087 | GEO

DYRK2 regulates cancer stem cell population.

Project description:We used microarrays to identified new factor that regulates cancer stem cell population in shRNA DYRK2 cells using stable DYRK2 knockdown cells and mammosphere. We stably silenced DYRK2 in MCF-7 cells (shRNA-DYRK2 cells) using pSuper vector. For control, pSuper control cells were created. We obtained expression profiles from shRNA-DYRK2 cells and pSuper control cells. We also obtained RNA from mammosphere which are stably expressing pSuper vector or shRNA DYRK2.

2016-08-23 | E-GEOD-75918 | biostudies-arrayexpress

Expression data of Brti1 shRNA knockdown and control shRNA in MCF-10A cells

Project description:Homologous recombination-mediated DNA repair deficiency (HRD) predisposes to cancer development, but also provides therapeutic opportunities Here, we identified an HRD gene signature that robustly predicted HRD status Unexpectedly, concurrent loss of PTEN in BRCA1-deficient cells might extensively rewire the HR repair network and confer resistance to PARP inhibitor, partially through over-expression of TTK We used the HRD gene signature as a drug discovery tool and found several PARP-inhibitor-synergizing agents through the connectivity map Thus gene expression profiling can be used to define the functional status of the HR repair network providing prognostic and therapeutic information Various shRNAs that target genes involved in homologous recombination (HR) were transfected in MCF-10A non-transformed breast cells lines Stable HR gene knockdown MCF-10A cells were seeded 200000 at 10 cm plate Cells were harvested after 48 hours culturing and used for gene expression profiling The shRNA that target Brit1 genes was transfected in MCF-10A non-transformed breast cell line by lentiviral particles and selected stable Brit1 knockdown MCF-10A cells. Scrambled control shRNA-transfected MCF-10A cells were applying as control. Both stable Brit1 knockdown and control MCF-10A cells were seeded with 2 x 10^5 cells at 10 cm culture plate. Cells were cultured in MCF-10A medium and harvested after 48 hours culturing. mRNA was extracted from collected cells and performing gene expression profiling. Three or four biological replicates were applied.

2014-01-24 | E-GEOD-54264 | biostudies-arrayexpress

RNAi profiling of human MCF-7 cells depleted for NAMPT knockdown

Project description:NAMPT is an enzyme in the mammalian NAD+ salvage pathway. Expression microarray analysis was used to study the effect of NAMPT knockdown on gene expression in MCF-7 breast cancer cells. Experiment Overall Design: Stable knockdown of NAMPT was achieved using a retroviral shRNA construct. An shRNA directed against Luciferase was used to generate the Luc control cells. Three independent biological replicates with matching Luc controls were analyzed using Affymetrix U133 A2.0 microarrays.

2009-06-08 | E-GEOD-13449 | biostudies-arrayexpress

Expression data of BRCA1 shRNA and PTEN shRNA single knockdown, BRCA1_PTEN shRNA double knockdowns and control shRNA in MCF-10A cells

Project description:Homologous recombination-mediated DNA repair deficiency (HRD) predisposes to cancer development, but also provides therapeutic opportunities. Here, we identified an HRD gene signature that robustly predicted HRD status. Unexpectedly, concurrent loss of PTEN in BRCA1-deficient cells might extensively rewire the HR repair network and confer resistance to PARP inhibitor, partially through over-expression of TTK. We used the HRD gene signature as a drug discovery tool and found several PARP-inhibitor-synergizing agents through the connectivity map. Thus gene expression profiling can be used to define the functional status of the HR repair network providing prognostic and therapeutic information. Various shRNAs that target genes involved in homologous recombination (HR) were transfected in MCF-10A non-transformed breast cells lines. Stable HR gene knockdown MCF-10A cells were seeded 200000 at 10 cm plate. Cells were harvested after 48 hours culturing and used for gene expression profiling. The shRNAs that target PTEN or BRCA1 genes were transfected in MCF-10A non-transformed breast cell line by lentiviral particles to generate either single gene knockdown or double gene knockdown. Stable BRCA1, PTEN, and BRCA1_PTEN MCF-10A cells were selected. Scrambled control shRNA-transfected MCF-10A cells were applying as control. All knockdown and control MCF-10A cells were seeded with 2 x 10^5 cells at 10 cm culture plate. Cells were cultured in MCF-10A medium and harvested after 48 hours culturing. mRNA was extracted from collected cells and performing gene expression profiling. Three or four biological replicates were applied. Four biological replicates were applied.

2014-01-24 | E-GEOD-54265 | biostudies-arrayexpress

Expression data of BRCA1 shRNA and Rad51 shRNA knockdown and control shRNA in MCF-10A cells

Project description:Homologous recombination-mediated DNA repair deficiency (HRD) predisposes to cancer development, but also provides therapeutic opportunities. Here, we identified an HRD gene signature that robustly predicted HRD status. Unexpectedly, concurrent loss of PTEN in BRCA1-deficient cells might extensively rewire the HR repair network and confer resistance to PARP inhibitor, partially through over-expression of TTK. We used the HRD gene signature as a drug discovery tool and found several PARP-inhibitor-synergizing agents through the connectivity map. Thus gene expression profiling can be used to define the functional status of the HR repair network providing prognostic and therapeutic information. Various shRNAs that target genes involved in homologous recombination (HR) were transfected in MCF-10A non-transformed breast cells lines. Stable HR gene knockdown MCF-10A cells were seeded 200000 at 10 cm plate. Cells were harvested after 48 hours culturing and used for gene expression profiling. The shRNAs that target PTEN or BRCA1 genes were transfected in MCF-10A non-transformed breast cell line by lentiviral particles. Stable BRCA1 and PTEN knockdown MCF-10A cells were selected. Scrambled control shRNA-transfected MCF-10A cells were applying as control. All knockdown and control MCF-10A cells were seeded with 2 x 10^5 cells at 10 cm culture plate. Cells were cultured in MCF-10A medium and harvested after 48 hours culturing. mRNA was extracted from collected cells and performing gene expression profiling. Four biological replicates were applied. Four biological replicates were applied.

2014-01-24 | E-GEOD-54266 | biostudies-arrayexpress

Expression data of ATM, ATR, CHK1, CHK2, and 53BP1 shRNA knockdown and control shRNA in MCF-10A cells

Project description:Homologous recombination-mediated DNA repair deficiency (HRD) predisposes to cancer development, but also provides therapeutic opportunities. Here, we identified an HRD gene signature that robustly predicted HRD status. Unexpectedly, concurrent loss of PTEN in BRCA1-deficient cells might extensively rewire the HR repair network and confer resistance to PARP inhibitor, partially through over-expression of TTK. We used the HRD gene signature as a drug discovery tool and found several PARP-inhibitor-synergizing agents through the connectivity map. Thus gene expression profiling can be used to define the functional status of the HR repair network providing prognostic and therapeutic information. Various shRNAs that target genes involved in homologous recombination (HR) were transfected in MCF-10A non-transformed breast cells lines. Stable HR gene knockdown MCF-10A cells were seeded 200000 at 10 cm plate. Cells were harvested after 48 hours culturing and used for gene expression profiling. The shRNAs that target ATM, ATR, CHK1, CHK2, and 53BP1 genes were transfected in MCF-10A non-transformed breast cell line by lentiviral particles and selected stable ATM, ATR, CHK1, CHK2, and 53BP1 knockdown MCF-10A cells. Scrambled control shRNA-transfected and wild type MCF-10A cells were applying as control. All knockdown and control MCF-10A cells were seeded with 2 x 10^5 cells at 10 cm culture plate. Cells were cultured in MCF-10A medium and harvested after 48 hours culturing. mRNA was extracted from collected cells and performing gene expression profiling. Three biological replicates were applied.

2014-01-24 | E-GEOD-54268 | biostudies-arrayexpress

Expression data of CHK1 shRNA knockdown and control shRNA in U2OS cells

Project description:Homologous recombination-mediated DNA repair deficiency (HRD) predisposes to cancer development, but also provides therapeutic opportunities. Here, we identified an HRD gene signature that robustly predicted HRD status. Unexpectedly, concurrent loss of PTEN in BRCA1-deficient cells might extensively rewire the HR repair network and confer resistance to PARP inhibitor, partially through over-expression of TTK. We used the HRD gene signature as a drug discovery tool and found several PARP-inhibitor-synergizing agents through the connectivity map. Thus gene expression profiling can be used to define the functional status of the HR repair network providing prognostic and therapeutic information. Various shRNAs that target genes involved in homologous recombination (HR) were transfected in MCF-10A non-transformed breast cells lines. Stable HR gene knockdown MCF-10A cells were seeded 200000 at 10 cm plate. Cells were harvested after 48 hours culturing and used for gene expression profiling. The shRNA that target CHK1 gene was transfected in human osteosarcoma U2OS cell line by lentiviral particles and selected stable CHK1 knockdown U2OS cells. Scrambled control shRNA-transfected U2OS cells were applying as control. Both stable CHK1 knockdown and control U2OS cells were seeded with 2 x 10^5 cells at 10 cm culture plate. Cells were cultured in McCOY 5A medium with 10% FBS and harvested after 48 hours culturing. mRNA was extracted from collected cells and performing gene expression profiling. Three biological replicates were applied.

2014-01-24 | E-GEOD-54267 | biostudies-arrayexpress

RNAi knock down of AURKA in human neuroblastoma IMR-32 cells

Project description:IMR-32 cells were infected either with control-shRNA or one of two different AURKA-shRNA vectors to identify genes regulated after AURKA knockdown.

2008-06-01 | E-MEXP-1496 | biostudies-arrayexpress

Study of SPEN knockdown in MCF-7 cells. (2)

Project description:We investigated the functions/pathways affected by SPEN knockdown in breast cancer by global expression profiling in a cell model, where the human breast cancer cell line, MCF-7, were transfected with an shRNA targeting SPEN mRNA.

2015-10-21 | E-MTAB-2183 | biostudies-arrayexpress

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