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HeLa/16E6 Cells (Wild-type E2-infected vs. Mutant E2-infected)

ABSTRACT: Senescent HeLa/16E6 cells compared to proliferating HeLa/16E6 cells Keywords: Wild-type E2 Infection vs. Mutant E2 Infection

ORGANISM(S): Homo sapiens

PROVIDER: GSE6759 | GEO | 2007/01/24

SECONDARY ACCESSION(S): PRJNA104203

REPOSITORIES: GEO

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HeLa/16E6-16E7d21-24 Cells (Wild-type E2-infected vs. Mutant E2-infected)

Project description:Senescent HeLa/16E6-16E7d21-24 cells compared to proliferating HeLa/16E6-16E7d21-24 cells Keywords: Wild-type E2 Infection vs. Mutant E2 Infection

2007-01-24 | GSE6761 | GEO

HeLa/16E6 Cells (Wild-type E2-infected vs. Mock-infected)

Project description:Senescent HeLa/16E6 cells compared to proliferating HeLa/16E6 cells Keywords: Wild-type E2 Infection vs. Mock Infection

2007-01-24 | GSE6758 | GEO

HeLa/16E6-16E7 Cells (Wild-type E2-infected vs. Mutant E2-infected)

Project description:HeLa/16E6-16E7 cells after expression of wild-type E2 compared to an E2 DNA-binding mutant Keywords: Wild-type E2 Infection vs. Mutant E2 Infection

2007-01-24 | GSE6760 | GEO

ERalpha ChIP-chip from HeLA-ER cells treated with E2

Project description:We are studying the mechanisms by which the estrogen receptor, ERalpha, is recruited to and regulates genes with a non-direct DNA binding. We performed ChIP-chip for ERalpha in E2 treated HeLa-ER cells, and looked at 19000 RefSeq genes to determine binding patterns of the receptor at promoters. The experiment was performed in duplicate. ChIP-chip biological replicates for Eralpha in E2 treated HeLa-ER cells are included.

2011-02-22 | E-GEOD-22099 | biostudies-arrayexpress

ERalpha ChIP-chip from HeLA-ER cells treated with E2

2011-02-22 | GSE22099 | GEO

Homo sapiens

Project description:HeLa/16E6 Cells (Wild-type E2-infected vs. Mutant E2-infected)

| PRJNA104203 | ENA

Homo sapiens

Project description:HeLa/16E6-16E7 Cells (Wild-type E2-infected vs. Mutant E2-infected)

| PRJNA104205 | ENA

Homo sapiens

Project description:HeLa/16E6-16E7d21-24 Cells (Wild-type E2-infected vs. Mutant E2-infected)

| PRJNA104199 | ENA

Homo sapiens

Project description:HeLa/16E6 Cells (Wild-type E2-infected vs. Mock-infected)

| PRJNA104201 | ENA

MCF7 Cells: Control siRNA -E2 vs. Control siRNA +E2, Control siRNA -E2 vs. PES1 siRNA -E2,Control siRNA -E2 vs. PES1 siRNA +E2

Project description:The initiation of breast cancer is associated with increased expression of tumor-promoting estrogen receptor M-NM-1 (ERM-NM-1) protein and decreased expression of tumor-suppressive ERM-NM-2 protein. However, the mechanism underlying this process is unknown. Here we show that Pescadillo/PES1, an estrogen-inducible protein that is over-expressed in breast cancer, can regulate the balance between ERM-NM-1 and ERM-NM-2. PES1 enhances transcriptional activity of ERM-NM-1 and reduces that of ERM-NM-2, and modulates many estrogen-responsive genes. Consistent with this regulation of ERM-NM-1 and ERM-NM-2 transcriptional activity, PES1 increases the stability of the ERM-NM-1 protein and decreases that of ERM-NM-2 through the ubiquitin-proteasome pathway, mediated by the carboxyl terminus of Hsc70-interacting protein (CHIP). Moreover, PES1 can transform normal human mammary epithelial cells and is required for estrogen-induced breast tumor growth in nude mice. Further analysis of clinical samples showed that expression of PES1 correlates positively with ERM-NM-1 expression and negatively with ERM-NM-2 expression, and predicts good clinical outcome in breast cancer. Our data demonstrate that PES1 contributes to breast tumor growth through regulating the balance between ERM-NM-1 and ERM-NM-2 and may be a better target for the development of drugs that selectively regulate ERM-NM-1 and ERM-NM-2 activities. Three samples: Control siRNA -E2 vs. Control siRNA +E2, Control siRNA -E2 vs. PES1 siRNA -E2,Control siRNA -E2 vs. PES1 siRNA +E2

2012-06-09 | E-GEOD-38621 | biostudies-arrayexpress

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