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Prevalent p53 gain-of-function mutants co-opt epigenetic pathways to drive cancer growth

ABSTRACT: Prevalent p53 gain-of-function mutants co-opt epigenetic pathways to drive cancer growth

PROVIDER: PRJNA254538 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR1508730.fastq.gz	Fastqsanger.gz
	SRR1508740.fastq.gz	Fastqsanger.gz
	SRR1508731.fastq.gz	Fastqsanger.gz
	SRR1508741.fastq.gz	Fastqsanger.gz
	SRR1508732.fastq.gz	Fastqsanger.gz

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Prevalent p53 gain-of-function mutants co-opt epigenetic pathways to drive cancer growth

Project description:We investigated the genomewide binding pattern of prevalent p53 gain-of-function (GOF) mutants by ChIP-seq, in a panel of breast cancer cell lines. We assessed the genomewide changes of H3K4me3 upon GOF p53 knockdown in MDA-MB-468 breast cancer cells bearing the p53 R273H mutation. This study uses ChIP-seq of H3K4me3 and histone H3 in wild-type or p53 R172H knock-in MEFs. Additionally, this study examines the transcriptome of wild-type or p53 R172H knock-in MEFs using polyA+ RNA-seq.

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Prevalent p53 gain-of-function mutants co-opt epigenetic pathways to drive cancer growth

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Gain-of-function p53 mutants co-opt chromatin pathways to drive cancer growth.

Project description:TP53 (which encodes p53 protein) is the most frequently mutated gene among all human cancers. Prevalent p53 missense mutations abrogate its tumour suppressive function and lead to a 'gain-of-function' (GOF) that promotes cancer. Here we show that p53 GOF mutants bind to and upregulate chromatin regulatory genes, including the methyltransferases MLL1 (also known as KMT2A), MLL2 (also known as KMT2D), and acetyltransferase MOZ (also known as KAT6A or MYST3), resulting in genome-wide increases of histone methylation and acetylation. Analysis of The Cancer Genome Atlas shows specific upregulation of MLL1, MLL2, and MOZ in p53 GOF patient-derived tumours, but not in wild-type p53 or p53 null tumours. Cancer cell proliferation is markedly lowered by genetic knockdown of MLL1 or by pharmacological inhibition of the MLL1 methyltransferase complex. Our study reveals a novel chromatin mechanism underlying the progression of tumours with GOF p53, and suggests new possibilities for designing combinatorial chromatin-based therapies for treating individual cancers driven by prevalent GOF p53 mutations.

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