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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE216273 | 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]

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

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

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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

RNAseq analysis of taxol and palbociclib combination in pancreatic cancer

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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.

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