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S-adenosylmethionine treatment affects histone methylation in prostate cancer cells

ABSTRACT: S-adenosylmethionine treatment affects histone methylation in prostate cancer cells

PROVIDER: PRJNA986576 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24997949_1.fastq.gz	Fastqsanger.gz
	SRR24997949_2.fastq.gz	Fastqsanger.gz
	SRR24997950_1.fastq.gz	Fastqsanger.gz
	SRR24997950_2.fastq.gz	Fastqsanger.gz
	SRR24997951_1.fastq.gz	Fastqsanger.gz

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S-adenosylmethionine treatment affects histone methylation in prostate cancer cells

Project description:S-adenosylmethionine represents a potent inhibitor of cancer cell proliferation, migration and invasion in vitro. The reason remains unclear. Here, we examined if treatment with exogenous SAM is capable of causing alterations in the methylation of the histone markers H3K4me3 and H3K27me3, which are both known to be important in the initiation and progression of prostate cancer.

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Treatment of prostate cancer cells with S-adenosylmethionine leads to genomewide alterations of transcription profiles.

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S-adenosylmethionine (SAM) changes DNA methylation patterns in prostate cancer cells

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Project description:AdoMet (S-adenosylmethionine) inhibits cancer cell proliferation and migration via epigenetic alterations. The aim of this study was to investigate whether AdoMet may cause alterations in miRNA expression profiles important for the initiation and progression of prostate cancer. PC-3 cells were treated with AdoMet prior to miRNA sequencing. 17 differentially expressed miRNAs were detected. Target gene prediction was performed by means of databases. Results were aligned to transcriptomic data. Bioinformatic analysis revealed upregulation of anticancerogenic genes, downregulation of cancerogenic-related processes and pathways. Knocking down hsa-miR-192-5p in PC-3 cells resulted in downregulation of cancer cell proliferation, thus confirming these results.

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KMT9 writes the histone mark H4K12me1 and controls metabolism and proliferation of castration-resistant prostate cancer cells

Project description:Posttranslational modifications of histones such as methylation regulate chromatin structure and gene expression. Methylation of histone lysine residues is generally performed by SET domain methyltransferases. Here, we identify the heterodimeric C21orf127/TRMT112 complex as a specific histone methyltransferase. Assembly of the seven-b-strand protein C21orf127 (also named Hemk2, N6amt1 or PrmC) with TRMT112 is essential to form an active enzyme, hereafter named KMT9 that writes the histone mark H4K12me1 in vitro and in vivo. The H4K12me1 mark is enriched at promoters of KMT9 target genes and co-localises with the active histone mark H4K12ac. By controlling expression of genes involved in energy metabolism, KMT9 regulates oxidative phosphorylation in androgen receptor-dependent and -independent prostate tumour cells. Importantly, KMT9 depletion severely affects proliferation of castration and enzalutamide-resistant prostate cancer cells and xenograft tumours. Together, our data link the writing of the H4K12me1 histone mark by KMT9 with KMT9-dependent gene expression, which in consequence regulates energy metabolism and proliferation. KMT9 executes these functions independently of androgen receptor and androgen signalling thus, providing a promising paradigm for the treatment of castration resistant prostate cancer.

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S-Adenosylmethionine treatment diminishes the proliferation of castration- resistant prostate cancer cells by modulating the expression of miRNAs

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Project description:This study examines the therapeutic plausibility of using universal methyl group donor S-adenosylmethionine (SAM) to block breast cancer development, growth, and metastasis. cancer. Anti-tumor and anti-metastatic activity of SAM was evaluated through a series of studies in vitro using two different human breast cancer cell lines and in vivo using a MDA-MB-231 xenograft model of breast cancer. The data shown in this array is obtained from control and SAM-treated MDA-MB-231 cell lines.

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Treatment of prostate cancer cells with S-adenosylmethionine leads to genomewide alterations of transcription profiles.

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