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Ac4c modifications down-regulation in macrophages promotes suppressive tumor microenvironment in HCC (RIP-Seq)

ABSTRACT: Ac4c modifications down-regulation in macrophages promotes suppressive tumor microenvironment in HCC (RIP-Seq)

PROVIDER: PRJNA945454 | ENA |

REPOSITORIES: ENA

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Ac4c modifications down-regulation in macrophages promotes suppressive tumor microenvironment in HCC (RIP-Seq)

Project description:Ac4C-binding RNAs were analyzed by imprinting RNA-sequencing of anti-Ac4C antibody-retrieved complexes from macrophages lysate. We then performed gene expression profiling analysis using data obtained from RIP-seq of peritoneal macrophages incubated with IFN-G

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Ac4c modifications down-regulation in macrophages promotes suppressive tumor microenvironment in HCC

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Project description:NAT10-catalyzed N4-acetylcytidine (ac4C) has emerged as a vital post-transcriptional modulator on the coding transcriptome by promoting mRNA stability. To explore the transcriptome-wide profile of ac4C modification, we mapped the locations of ac4C modification on wild-type (WT) hESCs and NAT10 KD hESCs by high-throughput ac4C RNA immunoprecipitation sequencing (ac4C-RIP-seq).

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ac4C RIP-seq analysis of AGS cells upon NAT10 knockout.

Project description:N4-acetylcytidine (ac4C), a conserved chemical modification in eukaryotic prokaryotes that is catalyzed by the N-acetyltransferase 10 (NAT10) enzyme, plays a crucial role in promoting mRNA stability and translation. However, the biological function and mechanisms of NAT10-mediated ac4C in human cancer were poorly defined. In order to investigate the regulatory mechanism of NAT10 in gastric cancer, we performed ac4C RIP-seq(acRIP-seq) analysis in AGS cells with NAT10 knockout compared with control in two repeats.

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Ac4c modifications down-regulation in macrophages promotes suppressive tumor microenvironment in HCC

Project description:To investigated how NAT10 inhibitor (Remodelin hydrobromide) affected the function of peritoneal macrophages , we treated peritoneal macrophages IFN y，Remodelin hydrobromide and Remodelin hydrobromide with IFN y. We then performed gene expression profiling analysis using data obtained from RNA-seq of peritoneal macrophages with four treaments

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ac4C RIP-seq analysis of AGS cells upon NAT10 knockout.

Project description:ac4C RIP-seq analysis of AGS cells upon NAT10 knockout.

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NAT10 modulates fatty acid metabolism of palmitate driven MCF7 in ac4C dependent manner

Project description:We show that non-toxic exogenous palmitate uptake in MCF7 cells promotes NAT10 expression and NAT10-dependent ac4C RNA modification. It was previously reported that NAT10 modulates the addition of ac4C on RNA transcripts in normal and cancer conditions. However, no study report the impact of NAT10 in palmitate driven cells. Here we performed RNA immunoprecipitation sequencing (RIP-seq) in palmitate loaded MCF7 knockdown with NAT10 siRNA. Based on the pathways and enrichment landscape identified. We found that ac4C peaks of fatty acid metabolic genes including ELOVL6, ACSL1, ACSL3, ACSL4, ACADSB and ACAT1 were significantly decreased upon knockdown with NAT10 siRNA. Overall, our results revealed the impact of NAT10 as a regulator of fatty acid metabolism in ac4C-dependent manner

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chemical ac4C sequencing (ac4C-seq) to identify mRNA ac4C sites

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