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Reduction N6AMT1-mediated 6mA DNA modification promotes tumor progression [RNA-seq]

ABSTRACT: Background: DNA N6-methyladenosine (6mA) as a novel epigenetic signaling modification in humans and has been implicated in progression and tumorigenesis of several cancers. However, the function and mechanisms of 6mA in breast cancer (BC), the most common cancer among women, are unclear. Methods: The clinical role of 6mA was investigated by immunohistochemical (IHC) staining and Kaplan-Meier analysis of BC and their normal tissues. 6mA immunoprecipitation (IP) sequencing, mRNA sequencing and bioinformatics analysis were used to screen and validate the direct targets of 6mA. Results: Decreases in N6AMT1 correlated with the extent of 6mA in BC tissues and predicted a worse overall survival of BC patients. Knockdown N6AMT1 markedly reduced 6mA in DNA and promoted the proliferation and migration of BC in vivo and in vitro, whereas overexpression of N6AMT1 had the opposite effect, indicating N6AMT1 is a functional methyltransferase for DNA 6mA and relates with gene transcription. Critical negative regulators of the cell cycle, such as RB1, P21, REST and TP53 were identified as targets of N6AMT1 in BC. Conclusion: These results suggest N6AMT1 enhances DNA 6mA levels to repress tumor progression via transcriptional regulation of cell cycle inhibitors.

ORGANISM(S): Homo sapiens

PROVIDER: GSE166576 | GEO | 2022/03/31

REPOSITORIES: GEO

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Reduction N6AMT1-mediated 6mA DNA modification promotes tumor progression [MeDIP-seq]

Project description:Background: DNA N6-methyladenosine (6mA) as a novel epigenetic signaling modification in humans and has been implicated in progression and tumorigenesis of several cancers. However, the function and mechanisms of 6mA in breast cancer (BC), the most common cancer among women, are unclear. Methods: The clinical role of 6mA was investigated by immunohistochemical (IHC) staining and Kaplan-Meier analysis of BC and their normal tissues. 6mA immunoprecipitation (IP) sequencing, mRNA sequencing and bioinformatics analysis were used to screen and validate the direct targets of 6mA. Results: Decreases in N6AMT1 correlated with the extent of 6mA in BC tissues and predicted a worse overall survival of BC patients. Knockdown N6AMT1 markedly reduced 6mA in DNA and promoted the proliferation and migration of BC in vivo and in vitro, whereas overexpression of N6AMT1 had the opposite effect, indicating N6AMT1 is a functional methyltransferase for DNA 6mA and relates with gene transcription. Critical negative regulators of the cell cycle, such as RB1, P21, REST and TP53 were identified as targets of N6AMT1 in BC. Conclusion: These results suggest N6AMT1 enhances DNA 6mA levels to repress tumor progression via transcriptional regulation of cell cycle inhibitors.

2022-03-31 | GSE166580 | GEO

Reduction N6AMT1-mediated 6mA DNA modification promotes tumor progression

Project description:Reduction N6AMT1-mediated 6mA DNA modification promotes tumor progression

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Reduction N6AMT1-mediated 6mA DNA modification promotes tumor progression [MeDIP-seq]

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Reduction N6AMT1-mediated 6mA DNA modification promotes tumor progression [RNA-seq]

Project description:Reduction N6AMT1-mediated 6mA DNA modification promotes tumor progression [RNA-seq]

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N6-Methyladenine DNA Modification in Human Genome

Project description:In human cells, 5-methylcytosine (5mC) DNA modification plays an important role in gene regulation. However, N6-methyladenine (6mA) DNA modification, which is predominantly present in prokaryotes, is considered to be absent in human genomic DNA. Here, using single molecule real-time (SMRT) sequencing on human blood, we show that DNA 6mA modification is extensively present in human genome, accounting for ~0.051% of the total adenines. [G/C]AGG[C/T] was the most significant motif associated with 6mA modification. 6mA sites are enriched in the exon coding regions and are associated with transcriptional activation. DNA N6-methyladenine and N6-demethyladenine modification in human are mediated by methyltransferase N6AMT1 and demethylase ALKBH1, respectively. The 6mA abundance is significantly lower in cancer tissues compared to adjacent normal tissues, which is accompanied with decreased N6AMT1 and increased ALKBH1 levels. Decrease of 6mA modification level stimulated tumorigenesis in human. Collectively, our results demonstrate that 6mA DNA modification is present in human tissues, and we describe a potential role of the N6AMT1/ALKBH1-6mA regulatory axis in the progression of human cancer.

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Abundant DNA 6mA methylation during early embryogenesis of zebrafish

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Cytosolic N6AMT1-dependent translation supports mitochondrial RNA processing [RNA-Seq]

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Cytosolic N6AMT1-dependent translation supports mitochondrial RNA processing to prevent double-stranded RNA accumulation

Project description:Mitochondrial biogenesis relies on both the nuclear and the mitochondrial genomes, and the mechanisms that support their coordinated expression are not fully understood. Improper mitochondrial DNA expression can lead to inborn error of metabolism, inflammation, and aging. Here, we investigate N6AMT1, a nucleo-cytosolic multi-substrate methyltransferase. We analyze genetic dependency, transcription, translation, and proteomic profiles of N6AMT1-depleted cells and report that N6AMT1 is necessary for the cytosolic translation of factors involved in mitochondrial RNA metabolism, including subunits of the mitochondrial RNase P. In the absence of N6AMT1, RNA processing and translation within mitochondria are impaired, while double-stranded RNA accumulates in mitochondrial RNA granules causing an interferon response. Our work highlights a cytosolic program required for proper mitochondrial biogenesis, with consequences on innate immunity.

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