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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE39417 | GEO | 2013/05/01

SECONDARY ACCESSION(S): PRJNA170843

REPOSITORIES: GEO

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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

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

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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

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.

2011-09-30 | GSE28007 | GEO

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]

2011-09-30 | GSE28006 | GEO

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

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

2013-05-01 | GSE37323 | GEO

Expression profile of the endocrine therapy resistant breast cancer cells LTED depleted of PBX1 or treated with the gamma-secretase inhibitor MRK003

2013-05-01 | GSE36928 | GEO

Expression profile of the endocrine therapy resistant breast cancer cells LTED depleted of PBX1 or treated with the gamma-secretase inhibitor MRK003

Project description:Analysis of the response to PBX1 deprivation either using an siRNA approach or using a chemicalcompound indirectly targeting it. Deprivation of PBX1 is hypothesized to be essential for the growth of endocrine therapy resistant breast cancer cells (LTED) Total RNA was obtained from cells treated with siPBX1 or a control siRNA. The second set contains RNA from cells treated with MRK003 or a control (DMSO).

2013-05-01 | E-GEOD-36928 | biostudies-arrayexpress

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