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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. Profiling of PBX1 cistrome in MCF7 breast cancer cells

ORGANISM(S): Homo sapiens

SUBMITTER: luca magnani

PROVIDER: E-GEOD-28007 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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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

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 [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 [mRNA profiling]

2011-09-30 | GSE28006 | GEO

RIME against PBX1 protein in P19.6 mouse embryonal carcinoma cells treated for 48 hours with all-trans retinoic acid

Project description:Identification of PBX1 interactors in P19.6 mouse embryonal carcinoma cells treated for 48 hours with all-trans retinoic acid.

2017-04-03 | PXD006158 | Pride

Pbx1-d Induces T cell Activation and a Decreased Apoptosis in Response to Retinoic Acids (RA)

Project description:The hypothesis was tested that the Pbx1-d isoform was responsible for the Sle1a.1 phenotypes in CD4+ T cells. Jurkat T cells were transfected with a lentiviral construct expressing Pbx1-d-GFP or control RFP. Pbx1-d over-expression reduced the percentage of late apoptotic cells in response to anti-CD3 and anti-CD28 stimulation as compared with control-Lin28-transfected cells. Overall, these data demonstrate that over-expression of Pbx1-d results in an activated/inflammatory phenotype and in a defective response to RA in Jurkat T cells, strongly suggesting that the increased expression of Pbx1-d is responsible for the Sle1a.1 phenotypes. Jurkat T cells (5 x 105 cells/ml) were transfected with an lentiviral (LV) vector expressing either control (RFP or Lin28) or Pbx1-d-GFP. Total RNA was extracted from GFP+ or RFP+ FACS-sorted Jurkat T cells transfected LV-GFP-Pbx1-d or LV-RFP, as well as non-transfected cells in 4 independent transfections per group.

2010-07-07 | E-GEOD-22799 | biostudies-arrayexpress

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 [mRNA profiling]

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

Expression data from control and Pbx1-null CMPs and GMPs

Project description:The capacity of the hematopoietic system to promptly respond to peripheral demands relies on adequate pools of progenitors able to transiently proliferate and differentiate in a regulated manner. However, little is known about factors that may restrain progenitor maturation to maintain their reservoirs. In addition to a profound defect in hematopoietic stem cell (HSC) self-renewal, conditional knockout mice for the Pbx1 proto-oncogene have a significant reduction in lineage-restricted progenitors, including common myeloid progenitors (CMPs) and, to a lesser extent, granulocyte-monocyte progenitors (GMPs). Through analysis of purified progenitor proliferation, differentiation capacity and transcriptional profiling, we demonstrate that in the absence of Pbx1 the CMP pool is reduced due to aberrantly rapid myeloid maturation, associated with decreased expression of Meis1 and its targets including Flt3. BM cells were obtained from multiple bones of individual three to five week old Tie2Cre+.Pbx1-/f or Tie2Cre+.Pbx1+/f control mice (4-5 biological replicates/group). CMPs and GMPs were sorted by flow cytometry according to the following markers: Lin-/c-Kit+/Sca-/CD34+/CD16/32int, and Lin-/c-Kit+/Sca-/CD34+/CD16/32high, respectively, prior to RNA extraction.

2013-03-31 | E-GEOD-30028 | biostudies-arrayexpress

CUT&Tag of mouse primary B cells transduced Pbx1 overexpression plasmid.

Project description:We performed the cleavage under targets and tagmentation (Cut & tag) assay followed by sequencing enriched DNA fragments to reveal the direct downstream targets of Pbx1. Firstly, we overexpressed Pbx1b with Pbx1b-IRES-GFP retrovirus in murine peripheral B cells to ensure the yields of DNA fragments. CUT & tag libraries were generated following instructions of the manufacturer’s protocol (Vazyme; cat TD901-01) and the Pbx1 antibody (CST; cat 4342) was used for signal enrichment.

2023-03-26 | E-MTAB-12769 | biostudies-arrayexpress

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