Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA226270 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Purpose: AURKA plays an important role in breast cancer development. Exploring the gene expression profiles regulated by AURKA will facilitate to understand the mechanism which is responsible for AURKA induced breast cancer development. Results: We found that 350 genes were significantly up-regulated during AURKA overexpression in MCF-10A cells, 346 genes were significantly down-regulated during AURKA overexpression in MCF-10A cells. Conclusions: Our study indicated that 696 differentially expressed genes might contribute to AURKA induced breast cancer development. MCF-10A cells overexpressed AURKA or the empty vector were subjected to RNA extraction. The resulted RNA samples were performed RNA-sequencing analyses of gene expression profiles.
2015-10-28 | E-GEOD-57931 | biostudies-arrayexpress
Project description:Purpose: AURKA plays an important role in breast cancer development. Exploring the gene expression profiles regulated by AURKA will facilitate to understand the mechanism which is responsible for AURKA induced breast cancer development. Results: We found that 350 genes were significantly up-regulated during AURKA overexpression in MCF-10A cells, 346 genes were significantly down-regulated during AURKA overexpression in MCF-10A cells. Conclusions: Our study indicated that 696 differentially expressed genes might contribute to AURKA induced breast cancer development.
2015-10-28 | GSE57931 | GEO
Project description:Gene expression profiles MCF-10A cells overexpressing MBD2
| PRJNA208362 | ENA
Project description:To investigate the mechanisms of PI3Kα-induced senescence, we performed a gene expression microarray analysis with MCF-10A/H and parental MCF-10A cells.
2018-11-28 | GSE123014 | GEO
Project description:To study the function of 14-3-3ζ, we established MCF-10A human mammary epithelial cells transduced with 14-3-3ζ (10A.ζ) and vector (10A.Vec) We performed gene expression profiling on 10A.ζ cells and 10A.Vec cells, and normalized to profiling of MCF-10A parental cells
2013-11-05 | GSE52032 | GEO
Project description:Whole genome sequencing (WGS) of MCF-10A cells without or with NFIB overexpression cultured at 30 or 75 days and 5-fluoracil-resistant or oxaliplatin-resistant MCF-10A cells with NFIB overexpression cultured at 75 days to investigate whether the oncogenic potential of NFIB is linked to its function in replication initiation.
2023-08-22 | GSE201866 | GEO
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
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
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