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Sequencing to Explore the Mechanism Network of N-acetyltransferase 10 (NAT10) Promoting Colorectal cancer in human colorectal cancer cell SW620 [RIP-seq]

ABSTRACT: 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 RIP-Transcriptome Sequencing in human colorectal cancer cell SW620.

ORGANISM(S): Homo sapiens

PROVIDER: GSE265992 | GEO | 2025/02/12

REPOSITORIES: GEO

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Sequencing to Explore the Mechanism Network of N-acetyltransferase 10 (NAT10) Promoting Colorectal cancer in human colorectal cancer cell SW620

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

Sequencing to Explore the Mechanism Network of N-acetyltransferase 10 (NAT10) Promoting Colorectal cancer in human colorectal cancer cell SW620 [ac4CRIP]

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

Quantitative proteomics analysis of acute myeloid leukemia cells after NAT10 knockdown

Project description:RNA modification represents an important post-transcriptional regulatory mechanism in acute myeloid leukemia (AML). Given that the critical function of ac4C in control RNA translation, we sought to investigate the global impact of ac4C on protein expression. To this end, we conducted tandem mass tag (TMT) labeling and quantitative proteomics in MOLM13 AML cells with or without the ac4c writer NAT10 silencing.

2024-08-26 | PXD055119 | Pride

PCBP1/2 and TDP43 Function As NAT10 Adaptors In ac4C Writer Complex Towards mRNAs in Mammalian Cells [acRIPseq]

Project description:Massive numbers of modified bases in mRNAs sculpt the epitranscriptome and play vital roles in RNA metabolism. The only known acetylated RNA modification, N-4-acetylcytidine (ac4C), is highly conserved across cell types and among species. Although the GCN5-related acetyltransferase 10 (NAT10) functions as an ac4C writer, the mechanism underlying the acetylation process is largely unknown. In this study, we identified the NAT10/PCBP/TDP43 complex as an mRNA ac4C writer in mammalian cells. We identified RNA-binding proteins (RBPs) affiliated with two different families, PCBP1/2 (poly(rC)-binding protein 1/2) and TDP43 (TAR DNA binding protein 43), as NAT10 adaptors for mRNA tethering and substrate selection. Knockdown of the adaptors resulted in decreased mRNA acetylation abundance in HEK293T cells, with globally reduced density in 5`-untranslated region (UTR) and coding sequence (CDS) and ablated cytidine-rich ac4C motifs. The adaptors also affect the ac4C sites by recruiting NAT10 to their binding sequences. The presence of the NAT10/PCBP/TDP43 complex in mouse testes highlights its potential physiological functions in vivo. These findings reveal the composition of the mRNA ac4C writer complex in mammalian cells and expand our knowledge of mRNA acetylation and ac4C site preferences.

2024-12-27 | GSE252075 | GEO

PCBP1/2 and TDP43 Function As NAT10 Adaptors In ac4C Writer Complex Towards mRNAs in Mammalian Cells [293T_acRIPseq]

2024-12-27 | GSE252076 | GEO

Transcriptomic ac4C profiling in NAT10 knockdown acute myeloid leukemia cells

Project description:RNA modification represents an important post-transcriptional regulatory mechanism in acute myeloid leukemia (AML), however the function and mechanism of RNA acetylation ac4C in AML remains elusive. Here, we report that NAT10, as the ac4C writing enzyme, plays a critical oncogenic function in AML and represents a promising therapeutic target for AML. To understand the mechanisms underlying the function of NAT10 as an RNA ac4C writer in AML, we profiled ac4C modification in the transcriptome of MOLM13 cells using a refined ac4C RNA immunoprecipitation and high throughput sequencing (RacRIP-seq) protocol, and performed systematic calibration with a modification-free control library generated from the in vitro- transcribed MOLM13 transcriptome (referred to as IVT control) to eliminate most of the false- positive signals. We also applied the RacRIP-seq in NAT10 knockdown and control MOLM13 cells to characterize NAT10 targets.

2024-08-26 | GSE246505 | GEO

Sequencing to Explore the Mechanism Network of N-acetyltransferase 10 (NAT10) Promoting Colorectal cancer in human colorectal cancer cell SW620

Project description:Sequencing to Explore the Mechanism Network of N-acetyltransferase 10 (NAT10) Promoting Colorectal cancer in human colorectal cancer cell SW620

| PRJNA1103189 | ENA

N4-acetylcytidine-dependent GLMP mRNA stabilization by NAT10 promotes head and neck squamous cell carcinoma metastasis and remodels tumor microenvironment through MAPK/ERK signaling pathway

Project description:N4-acetylcytidine (ac4C) is a posttransciptional RNA modification regulating in various important bioprocess. However, the role in human cancer, especially lymph node metastasis, remains largely unknown. Here, we showed NAT10, as the only “writer” of ac4C mRNA modification, was highly expressed in HNSCC patients with lymph node metastasis. High NAT10 levels in lymph node of HNSCC patients predicted poor overall survival. Moreover, we found the high expression of NAT10 was positively upregulated by NRF1 transcription factor. Gain and loss-of-function displayed that NAT10 promoted cell metastasis in mice. Mechanistically, NAT10 induced ac4C modification of GLMP and stabilized its mRNA, which triggered the activation of MAPK/ERK signaling pathway. Lastly, the NAT10’s specific inhibitor Remodelin could inhibit HNSCC tumorigenesis via 4-NQO-induced murine tumor model and remodel the tumor microenvironment, including angiogenesis, CD8+ T cell and Treg recruitment. These results demonstrated that NAT10 promoted lymph node metastasis of HNSCC via ac4C-dependent stabilization of GLMP transcript, providing a potential epitranscriptomic-targeted therapeutic strategy for HNSCC.

2023-08-08 | GSE239900 | GEO

Sequencing to Explore the Mechanism Network of N-acetyltransferase 10 (NAT10) Promoting Colorectal cancer in human colorectal cancer cell SW620 [ac4CRIP]

Project description:Sequencing to Explore the Mechanism Network of N-acetyltransferase 10 (NAT10) Promoting Colorectal cancer in human colorectal cancer cell SW620 [ac4CRIP]

| PRJNA1105099 | ENA

Lactylation of NAT10 promotes N4‐acetylcytidine modification on tRNASer-CGA-1-1 to boost oncogenic DNA virus KSHV reactivation

Project description:N4-acetylcytidine (ac4C), a conserved but recently rediscovered RNA modification on tRNAs, rRNAs and mRNAs, is catalyzed by N-acetyltransferase 10 (NAT10). Lysine acylation is a ubiquitous protein modification that controls protein functions. Our latest study demonstrates a NAT10-dependent ac4C modification, which occurs on the polyadenylated nuclear RNA (PAN) encoded by oncogenic DNA virus Kaposi's sarcoma-associated herpesvirus (KSHV), can induce KSHV reactivation from latency and activate inflammasome. However, it remains unclear whether a novel lysine acylation occurs in NAT10 during KSHV reactivation and how this acylation of NAT10 regulates tRNAs ac4C modification. Here, we showed that NAT10 was lactylated by α-tubulin acetyltransferase 1 (ATAT1), as a writer at the critical domain, to exert RNA acetyltransferase function and thus increase the ac4C level of tRNASer-CGA-1-1. Mutagenesis at the ac4C site in tRNASer-CGA-1-1 inhibited its ac4C modifications, translation efficiency of viral lytic genes, and virion production. Mechanistically, KSHV PAN orchestrated NAT10 and ATAT1 to enhance NAT10 lactylation, resulting in tRNASer-CGA-1-1 ac4C modification, eventually boosting KSHV reactivation. Our findings reveal a novel post-translational modification in NAT10, as well as expand the understanding about tRNA-related ac4C modification during KSHV replication, which may be exploited to design therapeutic strategies for KSHV-related diseases.

2024-06-17 | GSE248740 | GEO

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