RNA-seq analysis of mRNA expression profiles upon NAT10 depletion
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA748143 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR15195151_1.fastq.gz | Fastqsanger.gz | |||
| SRR15195151_2.fastq.gz | Fastqsanger.gz | |||
| SRR15195152_1.fastq.gz | Fastqsanger.gz | |||
| SRR15195152_2.fastq.gz | Fastqsanger.gz | |||
| SRR15195153_1.fastq.gz | Fastqsanger.gz |
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Project description:NAT10 (N-acetyltransferase-like protein) regulates N4-acetylcytidine formation in RNA. However, the biological function and mechanisms of NAT10 were poorly defined. To understand the molecular mechanism by which NAT10 affect GC progression, we performed RNA sequencing (RNA-seq) in AGS cells with NAT10 knockout and in BGC823 cells with shNAT10, with independent biological replicates.
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Project description:NAT10 is an RNA cytidine transferase known to add acetyl group on RNA transcripts thereby promoting translational efficiency. It was reported that NAT10 regulates epithelial to mesenchymal transition (EMT), DNA damage, and cell proliferation in cancers. However, weather NAT10 regulates other crucial pathways is unknown. In our study we conducted gene expression profiling analysis using data obtained from RNA-seq of MCF7 NAT10 KO and scramble control. High throughput sequencing revealed fatty acid metabolism as the top enriched pathway with fatty acid metabolic genes such ELOVL6, ACSL1, ACSL3, ACSL4, ACADSB, and ACAT1 were found to be differentially down-regulated. Overall our results revealed NAT10 depletion suppresses fatty acid metabolism in MCF7.
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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.
2024-07-07 | GSE180494 | GEO
Project description:The diverse RNA modifications play essential functions in gene expression regulation. Aberrant RNA modifications are frequently associated with cancers, while the underlying mechanisms and clinical significance remain poorly understood. Here we revealed that the ac4C RNA acetyltransferase NAT10 is significantly upregulated in esophageal cancers (ESCA) and associated with poor ESCA prognosis. In addition, using cancer cell lines, xenograft tumor models, Nat10 conditional knockin and conditional knockout mice, in vivo ESCA tumorigenesis model and chemical inhibition approaches, we uncovered the critical physiological functions of NAT10 in promoting esophageal cancer tumorigenesis and progression in vitro and in vivo. Mechanistically, NAT10 depletion reduced the abundance of ac4C-modified tRNAs and significantly decreased the translation efficiencies of mRNAs enriched for ac4C-modified-tRNA decoded codons. We further identified EGFR as a key downstream target that facilitates NAT10’s oncogenic functions in promoting esophageal cancer progression. In terms of clinical significance, we demonstrated that NAT10 promotes esophageal cancer resistance to EGFR inhibitor gefitinib, and combination of NAT10 depletion and gefitinib treatment synergistically inhibits esophageal cancer progression in vitro and in vivo. Our data uncovered novel molecular mechanisms underlying esophageal cancer progression at the layer of mRNA translation control and provided molecular insights for development of effective cancer therapeutic strategies.
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Project description:We performedacRIP-seq between control CRC cells and CRC cells with NAT10 knockdown to identify NAT10 mediates mRNA ac4C modification
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Project description:Here, we show that NAT10 is an essential regulator of cellular plasticity, and its catalyzed mRNA cytidine acetylation represents a new layer of epitranscriptomic modulation.
2023-11-14 | PXD036888 | Pride
Project description:Despite the advance in diagnosis and treatment, the prognosis of osteosarcoma patients remains unsatisfied. Therefore, it is imperative to identify novel therapeutic targets for osteosarcoma. Through RNA sequencing (RNA-seq) combined with functional screening, N4-acetylcytidine (ac4C) acetyltransferase 10 (NAT10) was identified as a candidate therapeutic target in osteosarcoma. Upregulated NAT10 correlated with poor prognosis in osteosarcoma patients and NAT10 knockout drastically inhibited cell proliferation and metastasis in vitro and in vivo. NAT10 enhanced mRNA stability and translation efficiency of activating transcription factor 4 (ATF4) through ac4C modification. ATF4 induced transcription of asparagine synthetase (ASNS), which catalyzes asparagine (Asn) biosynthesis. Asn promote protein and nucleotide synthesis, facilitating osteosarcoma progression. Overexpression of ATF4, ASNS or supplementation of asparagine rescue the tumor inhibitory effect of NAT10 knockout.
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Project description:Glomerular endothelial cell mRNA profiles in mice with podocyte depletion
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Project description:Mammalian oocyte maturation is driven by strictly translational regulation of maternal mRNAs stored in the cytoplasm. However, the function and mechanism of post-transcriptional chemical modifications especially the newly identified N4-acetylcytidine (ac4C) catalyzed by N-acetyltransferase 10 (NAT10) in this process are previously unknown. In this study, we developed a low-input ac4C sequencing technology - ac4C LACE-seq and mapped 8241 ac4C peaks at the whole transcriptome level using 50 mouse oocytes at the germinal vesicle (GV) stage. We profiled the mRNA landscapes of NAT10-interactions and ac4C modifications. The NAT10-interacted and ac4C modified transcripts displayed association with high translation efficiency in oocytes. Oocyte-specific Nat10 knockout wiped out ac4C signals in oocytes and caused severe defects in meiotic maturation and female infertility. ac4C LACE-seq results indicated that Nat10 deletion led to a failure of ac4C deposition on mRNAs encoding key maternal factors such as MAY2, ZAR1, BTG4 and cyclin B1 that regulate transcriptome stability and maternal-to-zygotic transition. Nat10-deleted oocytes had decreased mRNA translation efficiencies during meiotic maturation, partially due to the direct inhibition ac4C sites on specific transcripts. In sum, we developed low-input, high-sensitivity mRNA ac4C profiling approach and highlighted the important physiological function of ac4C in precise regulation of the oocyte meiotic maturation by enhancing translation efficiency.
2024-08-26 | GSE253976 | GEO
Project description:Mammalian oocyte maturation is driven by strictly translational regulation of maternal mRNAs stored in the cytoplasm. However, the function and mechanism of post-transcriptional chemical modifications especially the newly identified N4-acetylcytidine (ac4C) catalyzed by N-acetyltransferase 10 (NAT10) in this process are previously unknown. In this study, we developed a low-input ac4C sequencing technology—ac4C LACE-seq and mapped 8241 ac4C peaks at the whole transcriptome level using 50 mouse oocytes at the germinal vesicle (GV) stage. We profiled the mRNA landscapes of NAT10-interactions and ac4C modifications. The NAT10-interacted and ac4C modified transcripts displayed association with high translation efficiency in oocytes. Oocyte-specific Nat10 knockout wiped out ac4C signals in oocytes and caused severe defects in meiotic maturation and female infertility. ac4C LACE-seq results indicated that Nat10 deletion led to a failure of ac4C deposition on mRNAs encoding key maternal factors such as MAY2, ZAR1, BTG4 and cyclin B1 that regulate transcriptome stability and maternal-to-zygotic transition. Nat10-deleted oocytes had decreased mRNA translation efficiencies during meiotic maturation, partially due to the direct inhibition ac4C sites on specific transcripts. In sum, we developed low-input, high-sensitivity mRNA ac4C profiling approach and highlighted the important physiological function of ac4C in precise regulation of the oocyte meiotic maturation by enhancing translation efficiency.
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