The effects of RNA binding activity and acetyltransferase enzyme activity of NAT10 on heart development
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE274008 | GEO | 2025/08/04
REPOSITORIES: GEO
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Project description:The effects of RNA binding activity and acetyltransferase enzyme activity of NAT10 on heart development
| PRJNA1144452 | ENA
Project description:The enzyme N-acetyltransferase 10 (NAT10), known as the exclusive catalyst for N4-acetylcytidine (ac4C) modification, has been associated with various cellular processes, including tRNA acetylation, 18S rRNA biogenesis, mRNA stability, and translational efficiency. Despite extensive investigation into its molecular mechanisms in vitro, the physiological function of NAT10 under normal conditions has remained largely undefined. In this study, we found that the deficiency of NAT10 led to a disruption of T cell development at steady state, and identified a pivotal role for NAT10 in preserving the pathogenicity of naïve CD4+ T cells to induce adoptive transfer colitis. Mechanistically, the lack of NAT10 triggers the diminished stability of the anti-apoptotic gene Bag3, initiating a cascade of events that includes the upregulation of apoptosis-related genes and an accelerated rate of apoptosis in T cells. Our findings reveal a previously unrecognized role of the NAT10-ac4C-Bag3 axis in maintaining T cell homeostasis in vivo.
2025-03-12 | GSE284711 | GEO
Project description:The enzyme N-acetyltransferase 10 (NAT10), known as the exclusive catalyst for N4-acetylcytidine (ac4C) modification, has been associated with various cellular processes, including tRNA acetylation, 18S rRNA biogenesis, mRNA stability, and translational efficiency. Despite extensive investigation into its molecular mechanisms in vitro, the physiological function of NAT10 under normal conditions has remained largely undefined. In this study, we found that the deficiency of NAT10 led to a disruption of T cell development at steady state, and identified a pivotal role for NAT10 in preserving the pathogenicity of naïve CD4+ T cells to induce adoptive transfer colitis. Mechanistically, the lack of NAT10 triggers the diminished stability of the anti-apoptotic gene Bag3, initiating a cascade of events that includes the upregulation of apoptosis-related genes and an accelerated rate of apoptosis in T cells. Our findings reveal a previously unrecognized role of the NAT10-ac4C-Bag3 axis in maintaining T cell homeostasis in vivo.
2025-03-12 | GSE285309 | GEO
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 goal of this study is to investigate how NAT10 regulates heart development
2025-08-04 | GSE274007 | GEO
Project description:The goal of this study is to investigate how NAT10 regulates heart development in mice. mRNA profiles in hearts of Nat10flox/flox and cardiomyocyte-specific Nat10 knockout (Nat10-CKO) mice at 10 days old were generated by deep sequencing using Illumina novaseq x plus (n=3 for each group).
2025-08-04 | GSE295332 | GEO
Project description:N-acetyltransferase 10 (NAT10), the only known mRNA ac4C “writer,” plays a significant role in several human diseases, including CRC and gastric cancer. As NAT10 can activate or repress important signaling pathways, such as the EMT pathway, DNA damage repair, or apoptosis, by catalyzing the ac4C modification of oncogene mRNA, targeting NAT10 shows great potential for inhibiting cancer cell malignant progression in vitro and in vivo. This complex network of colorectal cancer progression mediated by NAT10 remains to be identified, which can expand cancer therapy options. To identify potential NAT10-regulated ac4C targets, we checked mRNA sequencing in human colorectal cancer cell SW620.
2025-02-12 | GSE264582 | GEO
Project description:N-acetyltransferase 10 (NAT10), the only known mRNA ac4C “writer,” plays a significant role in several human diseases, including CRC and gastric cancer. As NAT10 can activate or repress important signaling pathways, such as the EMT pathway, DNA damage repair, or apoptosis, by catalyzing the ac4C modification of oncogene mRNA, targeting NAT10 shows great potential for inhibiting cancer cell malignant progression in vitro and in vivo. This complex network of colorectal cancer progression mediated by NAT10 remains to be identified, which can expand cancer therapy options. To identify potential NAT10-regulated ac4C targets, we checked ac4CRIP Sequencing in human colorectal cancer cell SW620.
2025-02-12 | GSE265993 | GEO
Project description:Hepatocellular carcinoma (HCC) is characterized by high morbidity and mortality, withlimited effective treatment options. NAT10 is the only known acetyltransferase formRNA ac4C modification and is recognized as a biomarker for HCC, promoting itsprogression. However, the critical role of NAT10 in hepatocarcinogenesis remains tobe fully elucidated, and the identification of suitable small-molecule inhibitors targetingNAT10 is of great interest. Here, we report that NAT10 promotes HCC progression bystabilizing SMAD3 mRNA through ac4C modification. Clinically, NAT10 is highlyexpressed in HCC tissues and is significantly associated with poor prognosis.Functionally, NAT10 downregulation inhibits HCC cell proliferation, invasion, andepithelial-mesenchymal transition (EMT), while promoting anoikis in vitro.Additionally, NAT10 depletion significantly impairs tumor growth, metastasis, andhepatocarcinogenesis in vivo. Mechanistically, NAT10 enhances oncogene SMAD3mRNA stability via ac4C modification, thereby activating TGF-β signaling pathway.We also identify a novel small-molecule inhibitor, NAT10-2023, which effectivelyblocks NAT10 activity. Notably, NAT10-2023 treatment significantly reducesintracellular RNA ac4C modification levels and disrupts NAT10-RNA interactions,leading to suppressed tumor progression. Overall, NAT10 drives HCC progression viaSMAD3 mRNA stability regulation and NAT10-2023 could be a promising therapeuticcandidate for targeting NAT10 in cancer treatment.
2026-05-18 | GSE297856 | GEO
Project description:Hepatocellular carcinoma (HCC) is characterized by high morbidity and mortality, withlimited effective treatment options. NAT10 is the only known acetyltransferase formRNA ac4C modification and is recognized as a biomarker for HCC, promoting itsprogression. However, the critical role of NAT10 in hepatocarcinogenesis remains tobe fully elucidated, and the identification of suitable small-molecule inhibitors targetingNAT10 is of great interest. Here, we report that NAT10 promotes HCC progression bystabilizing SMAD3 mRNA through ac4C modification. Clinically, NAT10 is highlyexpressed in HCC tissues and is significantly associated with poor prognosis.Functionally, NAT10 downregulation inhibits HCC cell proliferation, invasion, andepithelial-mesenchymal transition (EMT), while promoting anoikis in vitro.Additionally, NAT10 depletion significantly impairs tumor growth, metastasis, andhepatocarcinogenesis in vivo. Mechanistically, NAT10 enhances oncogene SMAD3mRNA stability via ac4C modification, thereby activating TGF-β signaling pathway.We also identify a novel small-molecule inhibitor, NAT10-2023, which effectivelyblocks NAT10 activity. Notably, NAT10-2023 treatment significantly reducesintracellular RNA ac4C modification levels and disrupts NAT10-RNA interactions,leading to suppressed tumor progression. Overall, NAT10 drives HCC progression viaSMAD3 mRNA stability regulation and NAT10-2023 could be a promising therapeuticcandidate for targeting NAT10 in cancer treatment.
2026-05-18 | GSE297009 | GEO