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Homo sapiens

ABSTRACT: Transcriptomic analysis in breast cancer cell lines after CDK4/6 inhibition

PROVIDER: PRJNA387164 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5575220.fastq.gz	Fastqsanger.gz
	SRR5575230.fastq.gz	Fastqsanger.gz
	SRR5575221.fastq.gz	Fastqsanger.gz
	SRR5575231.fastq.gz	Fastqsanger.gz
	SRR5575222.fastq.gz	Fastqsanger.gz

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Effect of depletion of CDK4 on gene expression of MCF-7 breast cance cells

Project description:CDK4/6 inhibitors act as a cytostatic by targeting CDK4/6-cyclin D, and have achieved great success in hormone receptor-positive breast cancer treatment. Beyond cell cycle signaling pathway, recent research on non-cell cycle related functions of CDK4/6 has been blooming. Insights in this field may expand the therapeutic benefits of CDK4/6 inhibitors. Here, we attempt to explore the effects of CDK4/6 inhibitors on breast cancer from the perspective of epigenetic modifications, especially histone modifications, through high-throughput proteomic and genomics approaches. We reveal that inhibition of CDK4 directly suppresses phosphorylation of p300, an acetyltransferase, stimulates its ubiquitin degradation, and down-regulates the histone H3K27ac. Then, p300-mediated transcriptionally inhibition of BRCA1 and enrichment of breast cancer stem cells (BCSC) gene signatures lead to the increase of the proportion of ALDH1+ breast CSCs in ER+ breast cancer after long treatment with CDK4/6 inhibitors in vitro and in vivo. our results reveal a novel phosphorylation substrate of CDK4/cyclin D complex, and offer an unrecognized side effect of CDK4/6 inhibitors, inducing stem cell properties in ER+ breast cancer.

2024-09-17 | GSE261797 | GEO

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