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KMT9a writes the H4K12me1 histone mark and controls metabolism and proliferation of castration-resistant prostate cancer cells [RNA-seq]

ABSTRACT: The aim of the RNA-seq was to identify the KMT9 transcriptome in PC-3M cells. The MCF10A breast epithelial cells that do not express KMT9a were used to show that the siRNA against KMT9 show no off-target effects.

ORGANISM(S): Homo sapiens

PROVIDER: GSE117535 | GEO | 2019/06/26

REPOSITORIES: GEO

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

Project description:KMT9 is formed by the assembly of KMT9a and KMT9b and writes the H4K12me1 mark. The objectives of this study is to identify KMT9a, KMT9b, and H4K12me1 locations by ChIP-seq in the androgen-independent PC-3M prostate cancer cells and to show that upon KMT9a knockdown the levels of H4K12me1 mark decrease.

2019-06-26 | GSE117534 | GEO

KMT9 writes the H4K12me1 histone mark and controls metabolism and proliferation of castration-resistant prostate cancer cells [ChIP-Seq 2]

Project description:The aim of the study is to identify KMT9a target genes in PC-3M cells

2019-06-26 | GSE125882 | GEO

KMT9a writes the H4K12me1 histone mark and controls metabolism and proliferation of castration-resistant prostate cancer cells

Project description:This SuperSeries is composed of the SubSeries listed below. 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 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. We characterized the recognition mode of H4K12 by KMT9 that is formed by the assembly of KMT9a with KMT9b by solving the co-crystal structure. Genome-wide analyses revealed KMT9 and H4K12me1 enrichment at promoters of KMT9 target genes. By controlling expression of genes involved in cell cycle regulation, KMT9 regulates proliferation of 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 cell cycle 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.

2019-06-26 | GSE117536 | GEO

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.

2019-03-11 | PXD008965 | Pride

KMT9a writes the H4K12me1 histone mark and controls metabolism and proliferation of castration-resistant prostate cancer cells

Project description:KMT9a writes the H4K12me1 histone mark and controls metabolism and proliferation of castration-resistant prostate cancer cells

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Project description:Prostate cancer is the second-leading cause of cancer deaths for men in the U.SS. Global phosphorylation study on prostate cancer is still rare, in this study SILAC and TiO2 were used to quantify the phosphorylation in PC-3 cell and PC-3M cell. Global proteomics analysis was used to comparative analysis the protein level in the PC-3 cell and PC-3M cell.

2020-07-22 | PXD016282 | Pride

KMT9a writes the H4K12me1 histone mark and controls metabolism and proliferation of castration-resistant prostate cancer cells [RNA-seq]

Project description:KMT9a writes the H4K12me1 histone mark and controls metabolism and proliferation of castration-resistant prostate cancer cells [RNA-seq]

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

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.

2024-09-10 | E-MTAB-14388 | biostudies-arrayexpress

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

Project description:KMT9 writes the H4K12me1 histone mark and controls metabolism and proliferation of castration-resistant prostate cancer cells [ChIP-seq]

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