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RNA-seq transcriptome analyses in T47D cells treated with ActA and Palbociclib.

ABSTRACT: RNA-seq transcriptome analyses in T47D cells treated with ActA and Palbociclib.

PROVIDER: PRJNA482345 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7551083.fastq.gz	Fastqsanger.gz
	SRR7551084.fastq.gz	Fastqsanger.gz
	SRR7551085.fastq.gz	Fastqsanger.gz
	SRR7551086.fastq.gz	Fastqsanger.gz

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RNA-seq transcriptome analyses in T47D cells treated with ActA and Palbociclib.

Project description:We performed SMAD2 ChIP-seq analysis in T47D cells with/without Palbociclib treatment. To validate whether the changes in SMAD2 binding to the genome indeed resulted in changes in target gene expression, we performed RNA-seq transcriptome analyses in T47D with/without ActA stimulation and Palbo treatment.

2018-10-23 | GSE117497 | GEO

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

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

Gene expression analyses of palbociclib treated ER+ breast cancer cell lines as assessed by RNA-seq

Project description:The goal of this study is to measure gene expression changes resulting over time of palbociclib treatment of T47D, MCF7, and CAMA1 ER+ breast cancer cell lines.

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Genome wide transcriptome analysis of palbociclib or GSK3326595 treated A375 cells [Palbociclib_GSK_RNASeq]

Project description:RNA-seq was performed to compare the transcriptional programmes of A375 cells treated with Palbociclib or GSK3326595 compared to untreated cells 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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