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The pioneer factor PBX1 guides a distinct ERa signaling in breast cancer [ChIP-seq]

ABSTRACT: We profiled global PBX1 binding in MCF7 cells. The hypothesis tested was that PBX1 binds regions that recruit ERa following estradiol stimulation.

ORGANISM(S): Homo sapiens

PROVIDER: GSE28007 | GEO | 2011/09/30

SECONDARY ACCESSION(S): PRJNA141919

REPOSITORIES: GEO

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The pioneer factor PBX1 guides a distinct ERa signaling in breast cancer [ChIP-seq]

Project description:We profiled global PBX1 binding in MCF7 cells. The hypothesis tested was that PBX1 binds regions that recruit ERa following estradiol stimulation. Profiling of PBX1 cistrome in MCF7 breast cancer cells

2011-09-29 | E-GEOD-28007 | biostudies-arrayexpress

The pioneer factor PBX1 guides a distinct ERa signaling in breast cancer [mRNA profiling]

Project description:Effect of PBX1 silencing on global gene expression of MCF7 cells stimulated with estradiol. The hypothesis tested was that PBX1 is essential for estrogen signaling in ERa positive breast cancer cells. Total RNA was obtained from MCF7 cells treated with siRNA directed at PBX1 or an siControl for 72h. Cells were then stimulated with estradiol (E2) for 3h prior to RNA extraction.

2011-09-29 | E-GEOD-28006 | biostudies-arrayexpress

The pioneer factor PBX1 guides a distinct ERa signaling in breast cancer [mRNA profiling]

2011-09-30 | GSE28006 | GEO

The pioneer factor PBX1 guides a distinct ERa signaling in breast cancer

Project description:This SuperSeries is composed of the following subset Series: GSE28006: The pioneer factor PBX1 guides a distinct ERa signaling in breast cancer [mRNA profiling] GSE28007: The pioneer factor PBX1 guides a distinct ERa signaling in breast cancer [ChIP-seq] Refer to individual Series

2011-09-29 | E-GEOD-28008 | biostudies-arrayexpress

Expression profile of the endocrine therapy sensitive breast cancer cells MCF7 depleted of PBX1

Project description:Effect of PBX1 silencing on global gene expression of MCF7 cells stimulated with EGF. The hypothesis tested was that PBX1 is essential for EGF signaling in ERa positive breast cancer cells. Total RNA was obtained from MCF7 cells treated with siRNA directed at PBX1 or an siControl for 72h. Cells were then stimulated with estradiol (EGF) for 3h prior to RNA extraction.

2013-05-01 | E-GEOD-39417 | biostudies-arrayexpress

The pioneer factor PBX1 guides a distinct ERa signaling in breast cancer [mRNA profiling]

Project description: Not available

| S-ECPF-GEOD-28006 | biostudies-other

Expression profile of the endocrine therapy sensitive breast cancer cells MCF7 depleted of PBX1

2013-05-01 | GSE39417 | GEO

The pioneer factor PBX1 guides a distinct ERa signaling in breast cancer

Project description:This SuperSeries is composed of the SubSeries listed below.

2011-09-30 | GSE28008 | GEO

Genome-wide reprogramming of the chromatin landscape underlies endocrine therapy resistance in breast cancer

Project description:The estrogen receptor alpha (ERa) drives the growth of two-thirds of all breast cancers. Endocrine therapy impinges on estrogen-induced ERa activation to block tumor growth. However, half of ERa-positive breast cancers are tolerant or acquire endocrine therapy resistance. Here we demonstrate that breast cancer cells undergo genome-wide reprogramming of their chromatin landscape, defined by epigenomic maps and chromatin openness, as they acquire resistance to endocrine therapy. This reveals a role for the Notch pathway while excluding classical ERa signaling. In agreement, blocking Notch signaling, using gamma-secretase inhibitors, or targeting its downstream gene PBX1 abrogates growth of endocrine therapy-resistant breast cancer cells. Moreover Notch signaling through PBX1 directs a transcriptional program predictive of tumor outcome and endocrine therapy response. Comparing histone modifications (H3K4me2 and H3K36me3), chromatin openness (FAIRE) and PBX1 binding between endocrine therapy sensitive MCF7 and resistant MCF7-LTED cells.

2013-05-01 | E-GEOD-37323 | biostudies-arrayexpress

FOXA and master transcription factors recruit Mediator and Cohesin to the core transcriptional regulatory circuitry of cancer cells

Project description:The Mediator and Cohesin complexes control the cellular transcriptional program. However, it is not well understood how they are recruited to regulatory regions. Our study shows that the core transcriptional regulatory circuitry of cancer cells is essential to recruit Mediator, Cohesin and NIPBL to enhancer and promoter regions of actively transcribed genes in cancer cells. ChIP-seq analysis of Mediator (MED1), Cohesin (SMC1A) and NIPBL in HEPG2, A549 and MCF7 cells. The analysis also includes ChIP-Seq data for the transcription factor ERa in MCF7 cells treated with estradiol.

2016-10-24 | E-GEOD-76893 | biostudies-arrayexpress

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