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PELP1 ChIP-chip from MCF-7 cells

ABSTRACT: Proline-, glutamic acid-, and leucine-rich protein 1 (PELP1) is a transcriptional coactivator that has previously been shown to collaborate with nuclear receptors. Evidence from other groups suggest that PELP1 may stimulate transcription by displacing the linker histone H1 and/or by recruiting the lysine demethylase KDM1 to demethylate H3K9me2. Also known as modulator of the non-genomic activity of estrogen receptor (MNAR), PELP1 has also been implicated promoting estrogen receptor signaling from the plasma membrane. We recently identified PELP1 a factor that interacts with the macro domain of the histone variant macroH2A1. To determine if PELP1 interacts with macroH2A1 in cells, we performed PELP1 ChIP-chip from MCF-7 cells. The pattern of PELP1 bind across the genome strongly correlates with that previously determined for macroH2A1. This data combined with additional experiments allow us to conclude that macroH2A1 regulates target gene expression in part by recruiting the transcriptional coregulator PELP1.

ORGANISM(S): Homo sapiens

PROVIDER: GSE22254 | GEO | 2014/04/24

SECONDARY ACCESSION(S): PRJNA128753

REPOSITORIES: GEO

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PELP1 ChIP-chip from MCF-7 cells

Project description:Proline-, glutamic acid-, and leucine-rich protein 1 (PELP1) is a transcriptional coactivator that has previously been shown to collaborate with nuclear receptors. Evidence from other groups suggest that PELP1 may stimulate transcription by displacing the linker histone H1 and/or by recruiting the lysine demethylase KDM1 to demethylate H3K9me2. Also known as modulator of the non-genomic activity of estrogen receptor (MNAR), PELP1 has also been implicated promoting estrogen receptor signaling from the plasma membrane. We recently identified PELP1 a factor that interacts with the macro domain of the histone variant macroH2A1. To determine if PELP1 interacts with macroH2A1 in cells, we performed PELP1 ChIP-chip from MCF-7 cells. The pattern of PELP1 bind across the genome strongly correlates with that previously determined for macroH2A1. This data combined with additional experiments allow us to conclude that macroH2A1 regulates target gene expression in part by recruiting the transcriptional coregulator PELP1. Two PELP1 ChIP-chip biological replicates from MCF-7 human breast cancer cells are included.

2014-04-24 | E-GEOD-22254 | biostudies-arrayexpress

Proline Glutamic acid and Leucine rich Protein 1 (PELP1) promotes glioblastoma progression by enhancing Wnt/β-catenin signaling

Project description:We examined the transcriptional changes modulated by Proline Glutamic acid and Leucine rich Protein 1 (PELP1) by performing global transcriptome analysis. U87 cells were transfected with control siRNA or PELP1 siRNA and the RNA was isolated and utilized for RNA-seq analysis. Our results demonstrated that PELP1 modulated genes were related to inhibition of matrix metalloproteases, glioma invasion signaling, Wnt/β-catenin signaling and other pathways related to invasion and GBM signaling.

2020-04-24 | GSE131502 | GEO

Cytoplasmic Localization of Proline, Glutamic Acid, Leucine-rich Protein 1 (PELP1) Induces Breast Epithelial Cell Migration through Up-regulation of Inhibitor of κB Kinase ϵ and Inflammatory Cross-talk with Macrophages

Project description:Cytoplasmic localization of proline, glutamic acid, leucine-rich protein 1 (PELP1) is observed in ∼40% of women with invasive breast cancer. In mouse models, PELP1 overexpression in the mammary gland leads to premalignant lesions and eventually mammary tumors. In preliminary clinical studies, cytoplasmic localization of PELP1 was seen in 36% of women at high risk of developing breast cancer. Here, we investigated whether cytoplasmic PELP1 signaling promotes breast cancer initiation in models of immortalized human mammary epithelial cells (HMECs). Global gene expression analysis was performed on HMEC lines expressing vector control, PELP1-wt, or mutant PELP1 in which the nuclear localization sequence was altered, resulting in cytoplasmic localization of PELP1 (PELP1-cyto). Global gene expression analysis identified that PELP1-cyto expression in HMECs induced NF-κB signaling pathways. Western blotting analysis of PELP1-cyto HMECs showed up-regulation of inhibitor of κB kinase ϵ (IKKϵ) and increased phosphorylation of the NF-κB subunit RelB. To determine whether secreted factors produced by PELP1-cyto HMECs promote macrophage activation, THP-1 macrophages were treated with HMEC-conditioned medium (CM). PELP1-cyto CM induced changes in THP-1 gene expression as compared with control cell CM. Double conditioned medium (DCM) from the activated THP-1 cells was then applied to HMECs to determine whether paracrine signaling from PELP1-cyto-activated macrophages could in turn promote migration of HMECs. PELP1-cyto DCM induced robust HMEC migration, which was reduced in DCM from PELP1-cyto HMECs expressing IKKϵ shRNA. Our findings suggest that cytoplasmic localization of PELP1 up-regulates pro-tumorigenic IKKϵ and secreted inflammatory signals, which through paracrine macrophage activation regulates the migratory phenotype associated with breast cancer initiation.

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MCF-7 cell RNA-seq analysis of PELP1-induced gene expression

Project description:RNA-seq was performed on MCF-7 cells expressing vector control (LXSN), PELP1-wt, and PELP1-cyto

2021-07-05 | GSE126776 | GEO

The therapeutic potential and significance of the PELP1 signaling pathway in hepatocellular carcinoma

Project description:We examined the significance and therapeutic potential of targeting PELP1 in Hepatocellular carcinoma. Total RNA were isolated from HEP3B-control Sh, and HEP3B-PELP1-Sh cells using RNeasy mini kit, and total RNA was isolated for RNA-seq analysis. Our results demonstrated that PELP1 knockdown regulates pathways related to inflammation and interferon signaling and downregulates several pathways including MYC and E2F.

2024-10-16 | GSE254860 | GEO

Global genomic and proteomic analysis of TNBC cells identifies the critical role of PELP1 in ribosome biogenesis

Project description:We examined the mechanisms by which PELP1 regulates TNBC progression. MDA-MB-231 cells were stably transfected with control non-targeted shRNA or PELP1 shRNA, and total RNA was isolated for RNA-seq analysis. Our results demonstrated that PELP1 regulates the expression of Myc, E2F and mTOR targets in TNBC.

2022-03-03 | GSE191066 | GEO

Progesterone receptor-B enhances estrogen responsiveness of breast cancer cells via scaffolding PELP1- and estrogen receptor-containing transcription complexes

Project description:Progesterone and estrogen are important drivers of breast cancer proliferation. Herein, we probed estrogen receptor-α (ER) and progesterone receptor (PR) cross-talk in breast cancer models. Stable expression of PR-B in PR-low/ER+ MCF7 cells increased cellular sensitivity to estradiol and insulin-like growth factor 1 (IGF1), as measured in growth assays performed in the absence of exogenous progestin; similar results were obtained in PR-null/ER+ T47D cells stably expressing PR-B. Genome-wide microarray analyses revealed that unliganded PR-B induced robust expression of a subset of estradiol-responsive ER target genes, including cathepsin-D (CTSD). Estradiol-treated MCF7 cells stably expressing PR-B exhibited enhanced ER Ser167 phosphorylation and recruitment of ER, PR and the proline-, glutamate- and leucine-rich protein 1 (PELP1) to an estrogen response element in the CTSD distal promoter; this complex co-immunoprecipitated with IGF1 receptor (IGFR1) in whole-cell lysates. Importantly, ER/PR/PELP1 complexes were also detected in human breast cancer samples. Inhibition of IGF1R or phosphoinositide 3-kinase blocked PR-B-dependent CTSD mRNA upregulation in response to estradiol. Similarly, inhibition of IGF1R or PR significantly reduced ER recruitment to the CTSD promoter. Stable knockdown of endogenous PR or onapristone treatment of multiple unmodified breast cancer cell lines blocked estradiol-mediated CTSD induction, inhibited growth in soft agar and partially restored tamoxifen sensitivity of resistant cells. Further, combination treatment of breast cancer cells with both onapristone and IGF1R tyrosine kinase inhibitor AEW541 was more effective than either agent alone. In summary, unliganded PR-B enhanced proliferative responses to estradiol and IGF1 via scaffolding of ER-α/PELP1/IGF1R-containing complexes. Our data provide a strong rationale for targeting PR in combination with ER and IGF1R in patients with luminal breast cancer.

2015-03-15 | GSE45643 | GEO

The Estrogen Receptor Co-Regulator Protein, Proline Glutamic Acid and Leucine Rich Protein 1 (PELP1) Mediates Estrogen Rapid Signaling and Neuroprotection in the Brain

Project description:We examined the role of PELP1 in E2-ER-mediated transcription in the hippocampus under conditions of GCI by perfroming global transcriptome analysis. E2-treated FLOX and PELP1 FBKO mice were subjected to GCI followed by 24 h reperfusion and the isolated RNA was utilized for RNA-seq analysis. Our results demonstrated that PELP1 is needed for optimal activation of E2-regulated genes following GCI. Total RNA was isolated from the hippocampus of ovariectomized FLOX and PELP1 FBKO mice (implanted with E2 mini pumps) that were subjected to GCI followed by 24 h reperfusion. Illumina TruSeq RNA Sample Preparation was performed following manufacturer's protocol. Samples were run on an Illumina HiSeq 2000 in duplicate. The combined raw reads were aligned to UCSC hg19 and genes were annotated by Tophat. Genes were annotated and quantified by HTSeq-DESeq pipeline.

2015-12-07 | E-GEOD-72136 | biostudies-arrayexpress

The Estrogen Receptor Co-Regulator Protein, Proline Glutamic Acid and Leucine Rich Protein 1 (PELP1) Mediates Estrogen Rapid Signaling and Neuroprotection in the Brain

2015-12-07 | GSE72136 | GEO

Targeting PELP1 reduces endometrial cancer progression via attenuation of ribosomal biogenesis

Project description:We examined the mechanisms by which SMIP34 regulates EEC progression. EEC cells (HEC-1-A) were treated with either vehicle or SMIP34 20µM for 24 hours, and total RNA was isolated for RNA-seq analysis. Our results demonstrated that PELP1 inhibition by SMIP34 reduces the expression of genes involved in ribosome biogenesis and translation.

2024-10-16 | GSE226850 | GEO

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