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MAT2A promotes reprogramming of the androgen response pathway in association with ERG and EZH2

ABSTRACT: MAT2A promotes reprogramming of the androgen response pathway in association with ERG and EZH2

PROVIDER: PRJEB89672 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR14998562.fastq.gz	Fastqsanger.gz
	ERR14998563.fastq.gz	Fastqsanger.gz
	ERR14998564.fastq.gz	Fastqsanger.gz
	ERR14998565.fastq.gz	Fastqsanger.gz
	ERR14998566.fastq.gz	Fastqsanger.gz

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MAT2A promotes reprogramming of the androgen response pathway in association with ERG and EZH2

Project description:To date there are very few tools to reverse the induced dedifferentiation program in CRPC and to improve the response to the androgen deprivation therapy. Here we report that MAT2A is an important oncogenic cofactor of ERG/EZH2 transcriptional reprogramming impacting significantly the androgenic pathway. Using RNA sequencing coupled with ATAC, here we reveal an important link between ERG/MAT2A and EZH2 that impact on AR signaling pathway. This aberrant epigenetic program can be reversed by MAT2A inhibition which establish a near physiologic AR transcriptional program. Targeting MAT2A alone or in combination with EZH2 inhibitors reverse stemness in multiple models including prostatospheres from human PDX and GEM models of aggressive prostate cancer. Targeting MAT2A enhance the sensitivity to the androgenic blockade by Enzalutamide and to EZH2 inhibitors

2023-07-15 | E-MTAB-12031 | biostudies-arrayexpress

MAT2A promotes reprogramming of the androgen response pathway in association with ERG and EZH2

2023-07-15 | E-MTAB-12029 | biostudies-arrayexpress

MAT2A promotes reprogramming of the androgen response pathway in association with ERG and EZH2

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MAT2A promotes reprogramming of the androgen response pathway in association with ERG and EZH2

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MAT2A promotes reprogramming of the androgen response pathway in association with ERG and EZH2 (ChIP-Seq)

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Epigenome-wide impact of MAT2A sustains the androgen-indifferent state and confers synthetic vulnerability in ERG fusion-positive prostate cancer

Project description:Castration-resistant prostate cancer (CRPC) is a frequently occurring disease with adverse clinical outcomes and limited therapeutic options. Here, we identify a novel role of methionine adenosyltransferase 2a (MAT2A) as a driver of the androgen-indifferent state in ERG fusion-positive CRPC. We show that MAT2A is upregulated in CRPC and cooperates with ERG in promoting cell plasticity, stemness and tumorigenesis. RNA, ATAC and ChIP sequencing coupled with mass spectrometry analysis of histone post-translational modifications show that MAT2A broadly impacts the transcriptional and epigenetic landscape. MAT2A enhances H3K4me2 at multiple genomic sites promoting the expression of pro-tumorigenic non-canonical AR target genes in CRPC models. Genetic and pharmacological inhibition of MAT2A in preclinical models reversed this transcriptional and epigenetic remodeling, promoting luminal differentiation and improving the response to AR and EZH2 inhibitors. This data reveals a previously unrecognized function of MAT2A in epigenetic reprogramming and a synthetic vulnerability to MAT2A inhibitors in ERG fusion-positive CRPC.

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MAT2A promotes reprogramming of the androgen response pathway in association with ERG and EZH2

Project description:MAT2A promotes reprogramming of the androgen response pathway in association with ERG and EZH2

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MAT2A promotes reprogramming of the androgen response pathway in association with ERG and EZH2

Project description:MAT2A promotes reprogramming of the androgen response pathway in association with ERG and EZH2

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MAT2A promotes reprogramming of the androgen response pathway in association with ERG and EZH2

Project description:MAT2A promotes reprogramming of the androgen response pathway in association with ERG and EZH2

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MAT2A promotes reprogramming of the androgen response pathway in association with ERG and EZH2 (ChIP-Seq)

Project description:MAT2A promotes reprogramming of the androgen response pathway in association with ERG and EZH2 (ChIP-Seq)