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Palbociclib releases the latent differentiation capacity of neuroblastoma cells [H3K27ac ChIP-seq palbociclib]

ABSTRACT: We have used H3K27ac ChIP-seq to assess the global impact of palbociclib on the epigenetic H3K27ac landscape in three neuroblastoma cell lines.

ORGANISM(S): Homo sapiens

PROVIDER: GSE216291 | GEO | 2023/08/15

REPOSITORIES: GEO

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Palbociclib releases the latent differentiation capacity of neuroblastoma cells [H3K27ac ChIP-seq PB and RA]

Project description:We have used H3K27ac ChIP-seq to assess the global impact of the combination of palbociclib and retinoic acid on the epigenetic H3K27ac landscape in three neuroblastoma cell lines.

2023-08-15 | GSE236052 | GEO

Palbociclib releases the latent differentiation capacity of neuroblastoma cells [RNA-seq PB]

Project description:We have used RNA-seq to assess the global impact of palbociclib on the transcriptome at early and late time points in three neuroblastoma cell lines.

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Palbociclib releases the latent differentiation capacity of neuroblastoma cells [RNA-seq PB and RA]

Project description:We have used RNA-seq to assess the global impact of palbociclib, retinoic acid and the combined treatment on the transcriptome.

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Palbociclib releases the latent differentiation capacity of neuroblastoma cells

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

2023-08-15 | GSE216292 | GEO

H3K27ac, H3K4me and H3K4me3 binding examined by ChIP-seq in the CHP-134 neuroblastoma cell line

Project description:Super-enhancers are defined by peaks in H3K27 acetylation and H3K4 mono-methylation, and the lack of H3K4 tri-methylation. They have been found to play a role in oncogene transcription and tumour maintenance. Using ChIP-Seq, we profiled H3K27ac, H3K4me and H3K4me3 binding in CHP-134 neuroblastoma cells. We identified H3K27ac, H3K4me and H3K4me3 binding sites in the CHP-134 neuroblastoma cell line.

2019-06-23 | GSE113139 | GEO

Epigenetic subtypes of neuroblastoma [neuroblastoma]

Project description:In the absence of recurrent gene mutations, evidence accumulates that epigenetic deregulation plays a prominent role in neuroblastoma biology. Here we provide genome wide H3K27ac profiles in 60 primary neuroblastoma samples.

2020-09-16 | GSE135756 | GEO

Epigenomic profiling of neuroblastoma cell lines

Project description:Understanding the aberrant transcriptional landscape of neuroblastoma is necessary to provide insight to the underlying influences of the initiation, progression and persistence of this developmental cancer. Here, we present chromatin immunoprecipitation sequencing (ChIP-Seq) data for the oncogenic transcription factors, MYCN and MYC, as well as regulatory histone marks H3K4me1, H3K4me3, H3K27Ac, and H3K27me3 in ten commonly used human neuroblastoma-derived cell line models. In addition, for all of the profiled cell lines we provide ATAC-Seq as a measure of open chromatin. We validate specificity of global MYCN occupancy in MYCN amplified cell lines and functional redundancy of MYC occupancy in MYCN non-amplified cell lines. Finally, we show with H3K27Ac ChIP-Seq that these cell lines retain expression of key neuroblastoma super-enhancers (SE). We anticipate this dataset, coupled with available transcriptomic profiling on the same cell lines, will enable the discovery of novel gene regulatory mechanisms in neuroblastoma. This SuperSeries is composed of the SubSeries listed below.

2019-11-03 | GSE138315 | GEO

Brd4, H3K27Ac, and H3K36me3 binding profiles with or without Dinaciclib in human neuroblastoma CLB-GA cells

Project description:Promoter rearrangement of the telomerase reverse transcriptase (TERT) gene juxtaposes the coding sequence to strong enhancer elements, leading to TERT overexpression and poor prognosis. TERT associated oncogenic signaling in neuroblastoma remains unclear. Gene set enrichment analysis of RNA-seq data from 498 neuroblastoma patients revealed a coordinated activation of oncogenic signaling pathways and differentially overexpressed gene signature in a subgroup of MycN non-amplified neuroblastomas with TERT overexpression. ChIP-seq analysis of human neuroblastoma cell line CLB-GA harboring TERT rearrangement uncovered genome-wide chromatin co-occupancy of Brd4 and H3K27Ac and robust enrichment of H3K36me3 in TERT and multiple TERT-associated genes. We demonstrated a critical regulatory role of Brd4 and cyclin-dependent kinases in the expression and chromatin activation. Inhibition of both with AZD5153 and dinaciclib proved most effective in tumor growth suppression of neuroblastoma cell lines, primary cells, and xenograft. Our study provides a therapeutic strategy utilizing epigenetic targeting of neuroblastoma with TERT overexpression.

2020-05-12 | GSE133453 | GEO

Single cell RNA Seq to study the effects of Palbociclib in the mouse LSK cell compartment

Project description:To understand how Palbociclib (a CDK4/6 inhibitor) treatment changes the transcriptome of hematopoietic stem and progenitor cells, wildtype cells were isolated from mice and treated for 24h with either PBS (control) or Palbociclib. After 24h of culture, the cell suspensions were collected and sorted for lineage-negative, Sca1-positive, cKit-positive (LSK) cells which were subjected to library prep for single cell RNA sequencing.

2024-05-22 | E-MTAB-13268 | biostudies-arrayexpress

Gene expression alterations associated with acquired-resistance to the CDK4/6 inhibitor palbociclib [Palbociclib resistance_RNASeq]

Project description:RNA-seq was performed to compare the transcriptional programmes of palbociclib-resistant A375 and CHL1 cells compared to their parental counterparts Cyclin dependent kinase 4/6 (CDK4/6) inhibitors are an established treatment in estrogen receptor positive breast cancer and are currently in clinical development in melanoma; a tumour that exhibits high rates of CDK4 activation. We analyzed melanoma cells with acquired resistance to the CDK4/6 inhibitor palbociclib, and demonstrated that palbociclib-mediated inhibition of PRMT5 is essential for sensitivity to CDK4/6 inhibitors. Mechanistically, by inhibiting PRMT5 activity, palbociclib alters MDM4 pre-mRNA splicing leading to decreased MDM4 protein expression and subsequent p53 activation. In turn, p53 increases p21 leading to inhibition of CDK2, the main kinase substituting for CDK4/6 and a key driver of resistance to palbociclib. Loss of the ability of palbociclib to regulate the PRMT5-MDM4 axis leads to resistance. Importantly, combining palbociclib with the PRMT5 inhibitor GSK3326595 enhances the efficacy of palbociclib in treatment naïve and resistant models and also delays the emergence of resistance. Our studies have uncovered a novel mechanism of action of CDK4/6 inhibitors in regulating the MDM4 oncogene and the tumor suppressor, p53. Furthermore, we have established that palbociclib inhibition of the PRMT5-MDM4 axis is essential for robust melanoma cell sensitivity and provide pre-clinical evidence that co-inhibition of CDK4/6 and PRMT5 is an effective and well tolerated therapeutic strategy. Overall our data provides a strong rationale for further investigation of novel combinations of CDK4/6 and PRMT5 inhibitors in not only melanoma but other tumour types including breast, pancreatic and esophageal carcinoma.

2019-08-23 | GSE133567 | GEO

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