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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE236052 | GEO | 2023/08/15

REPOSITORIES: GEO

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

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

2023-08-15 | GSE216291 | GEO

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.

2023-08-15 | GSE216274 | 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.

2023-08-15 | GSE216273 | GEO

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

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

Gene expression profiles between the palbociclib monotherpy versus palbociclib alternating with ICI182,780 treatment in breast cancer cells at 10 weeks.

Project description:We examined differential gene expression profiles between MCF7 human breast cancer cells treated with vehicle alone (control), palbociclib monotherapy, palbociclib alternating with ICI182,780 treatment, and palbociclib resistant cells. For this, we used gene microarray expression profiling to identify significantly changed genes under different treatment conditions.

2023-04-10 | GSE229002 | GEO

RNA-seq of human breast cancer cell lines MCF7 and T74D naive and resistant to palbociclib treated with capivasertib, fulvestrant and combination

Project description:T47D and MCF7 cell lines were treated with long-term (continuous) palbociclib to induce 4 resistant cell-lines (T47D RB-, T47D CDK6H, MCF7 RB- and MCF7 PacqR). Each cell line (both parental and resistant) were then treated with DMSO (control), capivasertib monotherapy, fulvestrant monotherapy and capivasertib/fulvestrant combination. RNA data is available after each treatment and resistant cell lines additionally have RNA data available after continuous palbociclib treatment.

2023-08-14 | E-MTAB-13262 | biostudies-arrayexpress

Palbociclib interferes with origin firing in a pRb independent manner

Project description:Over the last decade, CDK4/6 inhibitors (palbociclib, ribociclib and abemaciclib) have emerged as promising anticancer drugs. Numerous studies have demonstrated that CDK4/6 inhibitors efficiently block the pRb-E2F pathway and induce cell cycle arrest in pRb-proficient cells. Based on these studies, the inhibitors have been approved by the FDA for treatment of advanced hormonal receptor (HR) positive breast cancers in combination with hormonal therapy. However, some evidence has recently shown unexpected effects of the inhibitors, promoting needs to understand more about the mechanism of inhibitors beyond pRb. Our study demonstrates here for the first time how palbociclib impairs the origin firing in the DNA replication process in pRb-deficient cell lines. Strikingly, despite the absence of pRb, cells treated with palbociclib synthesize less DNA without any induced cell cycle arrest. Furthermore, palbociclib treatment disturbs the temporal program of DNA replication and reduces the density of replication forks. Cells treated with palbociclib show a defect in the loading of proteins of the Pre-initiation complex (Pre-IC) on chromatin, indicating a reduced initiation of DNA replication. Our findings highlight hidden effects of palbociclib on the dynamics of DNA replication and on its cytotoxic consequences on cell viability in the absence of pRb. This study provides a potential therapeutic application of palbociclib to target genomic instability towards pRb deficient patient

2023-07-01 | GSE180530 | GEO

O-GlcNAcylation promotes Palbociclib resistance in breast cancer by regulating MITF nuclear translocation

Project description:Cyclin-dependent kinases 4 and 6 (CDK4/6) are essential drivers of the cell cycle and are also critical for the initiation and progression of diverse malignancies. Pharmacological inhibitors targeting CDK4/6 have demonstrated significant activity against various tumor types such as breast cancer. However, resistance to CDK4/6 inhibitors (CDK4/6i) (such as palbociclib) remains an immense obstacle in clinical and the underlying mechanisms have not been fully understood. Using quantitative high-throughput combinational screen (qHTCS) and genomic sequencing, we report that the Microphthalmia-associated transcription factor (MITF), was significantly elevated in palbociclib-resistance cells. Inhibition of MITF can enhance the therapeutic efficacy of Palbociclib and surmount Palbociclib resistance both in vitro and in vivo. Then we found that MITF is interacting with OGT in Palbociclib-resistance cells, and we also identified that Ser49 is the main O-GlcNAc site of MITF. O-GlcNAc of MITF is critical to mediated Palbociclib-resistance in cells.

2024-05-30 | PXD042763 | Pride

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