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

ABSTRACT: The initiation of breast cancer is associated with increased expression of tumor-promoting estrogen receptor α (ERα) protein and decreased expression of tumor-suppressive ERβ 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 ERα and ERβ. PES1 enhances transcriptional activity of ERα and reduces that of ERβ, and modulates many estrogen-responsive genes. Consistent with this regulation of ERα and ERβ transcriptional activity, PES1 increases the stability of the ERα protein and decreases that of ERβ 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 ERα expression and negatively with ERβ expression, and predicts good clinical outcome in breast cancer. Our data demonstrate that PES1 contributes to breast tumor growth through regulating the balance between ERα and ERβ and may be a better target for the development of drugs that selectively regulate ERα and ERβ activities. Three samples: Control siRNA -E2 vs. Control siRNA +E2, Control siRNA -E2 vs. PES1 siRNA -E2,Control siRNA -E2 vs. PES1 siRNA +E2

ORGANISM(S): Homo sapiens

SUBMITTER: long cheng

PROVIDER: S-ECPF-GEOD-38621 | biostudies-other |

REPOSITORIES: biostudies-other

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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 α (ERα) protein and decreased expression of tumor-suppressive ERβ 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 ERα and ERβ. PES1 enhances transcriptional activity of ERα and reduces that of ERβ, and modulates many estrogen-responsive genes. Consistent with this regulation of ERα and ERβ transcriptional activity, PES1 increases the stability of the ERα protein and decreases that of ERβ 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 ERα expression and negatively with ERβ expression, and predicts good clinical outcome in breast cancer. Our data demonstrate that PES1 contributes to breast tumor growth through regulating the balance between ERα and ERβ and may be a better target for the development of drugs that selectively regulate ERα and ERβ activities.

2012-06-10 | GSE38621 | GEO

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

Human MCF7 cells: Mock control vs. siRNA transfected against calreticulin

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Human MCF7 cells: Mock control vs. siRNA transfected against calreticulin

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Human MCF7 cells: Mock control vs. siRNA transfected against calreticulin

2013-02-26 | E-GEOD-44371 | biostudies-arrayexpress

siRIP140 and gene expression effects in E2-treated MCF7 cells

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Project description:We performed gene expression profiling on the MDA-MB-231 and MDA-MB-436 human breast cancer cell lines following siRNA-mediated inhibition of Fn14 expression as an approach to identify the mechanistic basis for Fn14 regulation of invasive capacity. Experiment Overall Design: Each cell lines was transfected with etiher an Fn14 or firefly luciferase-specific (GL2) siRNA, with untreated cells used as a reference. 2 biological replicates were performed for each array, independently grown, treated and harvested.

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SAS cells: control siRNA (siC) vs DDX3 siRNA (siD) transfected

Project description:Transcriptional profiling of SAS cells comparing siC-transfected SAS cells with siD-transfected SAS cells. The latter decreased proliferation and migration of SAS cells. Goal was to determine the DDX3-regulated transcripts.

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HT29 colon cancer cells: siRNA targeted gene knockdowns vs scrambled siRNA control or GFP siRNA control

Project description:Transcriptional profiling of HT29 colon cancer cells comparing siRNA-targeted knockdowns of glutaminase (GLUT), cytokeratin 20 (KER), DEAD/H box polypeptide 32 (DEAD), ribosomal protein L32 (RPL32) and transcription factor DP1 (TFDP1) versus scrambled siRNA control and GFP siRNA control Keywords: two-color spotted cDNA microarray, siRNA-targeted gene knockdowns

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