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Transcriptomic expression of A549 CDK2 KO cells treated or untreated with palbociclib

ABSTRACT: Transcriptomic expression of A549 CDK2 KO cells treated or untreated with palbociclib

PROVIDER: PRJNA811150 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18165623.fastq.gz	Fastqsanger.gz
	SRR18165624.fastq.gz	Fastqsanger.gz
	SRR18165625.fastq.gz	Fastqsanger.gz
	SRR18165626.fastq.gz	Fastqsanger.gz

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Transcriptomic expression of A549 CDK2 KO cells treated or untreated with palbociclib

Project description:Inducing senescence in cancer cells is emerging as a new therapeutic strategy. We tested the senescence induction of palbociclib in CDK2 KO cells, and profiled these for senescence associated gene signatures. This was a CRISPR generated CDK2 KO clone in A549 cells.

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RNA-seq data of wildtype, CDK2-knockdown and JUN-knockdown THP1 cells treated with LPS against untreated controls

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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.

2019-08-23 | GSE133568 | GEO

Transcriptomic expression of A549 cells treated with palbociclib and indisulam or PF-06873600 and SUM159 cells treated with PF-06873600

Project description:Inducing senescence in cancer cells is emerging as a new therapeutic strategy. We tested the senescence induction of palbociclib and indisulam or PF-06873600 in A549 and PF-06873600 in SUM159 cells, and profiled these for senescence associated gene signatures.

2022-03-03 | GSE197603 | GEO

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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Transcriptomic expression of A549 and SUM159 cells treated with palbociclib and indisulam

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A novel role of CDK2 inhibition in restraining microglial overactivation

Project description:Intrinsic immune checkpoints in microglia are vital for maintaining homeostatic immune response and preventing overactivation. Neuroinflammation, frequently driven by microglial overactivation, significantly influences a wide range of neurological disorders. While MEF2C has been associated with a syndromic form of autism spectrum disorder (ASD) and various other neurological disorders in humans, its specific role as an immune checkpoint remains poorly defined. By harnessing MEF2C-knockout (KO) induced microglia-like cells (iMGLs) through differentiation from human pluripotent stem cells (hPSCs), here we observed that these cells, following LPS stimulation, exhibited overactivation similar to patterns seen in various neurological disorders. High-throughput screening identified BMS265246, a CDK2 inhibitor, as effective in specifically suppressing the overactivated phenotypes of MEF2C-KO iMGLs, and in restoring inflammatory response closer to normal levels. Mechanistically, we uncovered that MEF2C regulates p21 transcription, a critical step in preventing CDK2 activation in microglia. Loss of MEF2C results in CDK2-induced RB phosphorylation and degradation, leading to enhanced NF-κB p65 subunit nuclear translocation and exacerbated inflammatory responses. Remarkably, BMS265246 treatment rectified microglial overactivation and ASD-like behaviors in both global and microglia-specific Mef2C heterozygous knockout mice. Overall, our findings elucidated a previously unknown immune checkpoint mechanism governed by MEF2C, and highlighted CDK2 as a potential key factor driving neuroinflammation through microglial overactivation. These insights positions CDK2 as a promising therapeutic target for treating various neurological diseases influenced by overactivated microglia.

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