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N-acetyltransferase 10 drives cisplatin chemoresistance by enhancing ac4C-associated DNA repair in bladder cancer

ABSTRACT: N-acetyltransferase 10 drives cisplatin chemoresistance by enhancing ac4C-associated DNA repair in bladder cancer

PROVIDER: PRJNA824002 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18654162_1.fastq.gz	Fastqsanger.gz
	SRR18654162_2.fastq.gz	Fastqsanger.gz
	SRR18654163_1.fastq.gz	Fastqsanger.gz
	SRR18654163_2.fastq.gz	Fastqsanger.gz
	SRR18654164_1.fastq.gz	Fastqsanger.gz

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N-acetyltransferase 10 drives cisplatin chemoresistance by enhancing ac4C-associated DNA repair in bladder cancer

Project description:To explore the molecular mechanism underlying NAT10-mediated cisplatin resistance in bladdder cancer, a genome-wide RNA-sequencing was conducted to compare gene expression profiles of T24 and UM-UC-3 cells with NAT10 knockdown and control. And acRIP-seq was performed to identified the downstream targets of NAT10.

2022-04-07 | GSE200285 | GEO

Targeted delivery of TGF-β inhibitor via LHRH-NanoTi reverses the NAT10/ac4C-mediated cisplatin-induced immunosuppressive tumor microenvironment in ovarian cancer

Project description:Background: Platinum-based chemotherapy for ovarian cancer is frequently compromised by the development of resistance, a process often accompanied by an immunosuppressive tumor microenvironment. The molecular mechanisms linking cisplatin resistance to immune evasion remain poorly understood, hindering the development of effective combination therapies. Results: This study reveals that cisplatin-induced immunosuppression and resistance are driven by a reduction in N-acetyltransferase 10 (NAT10)-mediated N4-acetylcytidine (ac4C) modification, which produces two parts of unfavorable effects: 1) activating the DNA damage repair pathway, thereby confers resistance to cisplatin; 2) enhancing the expression of TGF-β via NAT10's interaction with ribosomal proteins RPS3 and RPS6. The elevated TGF-β increases the infiltration of myeloid-derived suppressor cells (MDSCs), M2 macrophages, exhausted CD8+ T cells, and regulatory T cells (Tregs) within the tumor microenvironment. To target this pathway, we developed a LHRH receptor-targeted nanodelivery system for a TGF-β inhibitor, which synergized with cisplatin to achieve superior antitumor efficacy by effectively reversing the immunosuppressive microenvironment. Conclusions: Our study defines the NAT10/ac4C–TGF-β axis as a pivotal mechanism coordinating cisplatin resistance and immunosuppression in ovarian cancer. These findings propose targeted inhibition of TGF-β signaling as a promising therapeutic strategy to overcome platinum resistance by revitalizing the antitumor immune response.

2026-02-16 | GSE319188 | GEO

Targeted delivery of TGF-β inhibitor via LHRH-NanoTi reverses the NAT10/ac4C-mediated cisplatin-induced immunosuppressive tumor microenvironment in ovarian cancer [Ribo-Seq]

2026-02-18 | GSE318784 | GEO

Targeted delivery of TGF-β inhibitor via LHRH-NanoTi reverses the NAT10/ac4C-mediated cisplatin-induced immunosuppressive tumor microenvironment in ovarian cancer [RNA-Seq]

2026-02-18 | GSE318783 | GEO

Proteomic signature of neuroblastoma cells UKF-NB-4 reveals key role of lysosomal sequestration and the proteasome complex in acquiring chemoresistance to cisplatin

Project description:Cisplatin (CDDP) is a widely used agent in the treatment of neuroblastoma. Unfortunately, the development of acquired chemoresistance limits its clinical use. To gain a detailed understanding of the mechanisms underlying the development of such chemoresistance, we comparatively analysed established cisplatin-resistant neuroblastoma cell line (UKF-NB- 4CDDP) and its sensitive counterpart (UKF-NB-4). We confirmed the decreased sensitivity of tested cells to cisplatin and identified a cross-resistance to carboplatin and oxaliplatin. Among the proteins responsible for UKF-NB-4CDDP chemoresistance, ion channels transport family proteins, ABC superfamily proteins, SLC-mediated trans-membrane transporters, proteasome complex subunits and V-ATPases were identified. Moreover, we detected markedly higher proteasome activity in UKF-NB-4CDDP cells and a remarkable lysosomal enrichment that can be inhibited by bafilomycin A to sensitize UKF-NB-4CDDP to CDDP. Our results indicate that lysosomal sequestration and proteasome activity may be one of key mechanisms responsible for intrinsic chemoresistance of neuroblastoma to CDDP.

2019-01-02 | PXD012132 | Pride

transcriptome expression profiling of cisplatin chemoresistance 5-8F cells

Project description:transcriptome expression profiling of cisplatin chemoresistance 5-8F cells

| PRJNA557360 | ENA

NAT10-mediated ac4C-modification exacerbates ferroptosis by stabilizing HMOX1 in Deep vein thrombosis

Project description:In our study, we aimed to identify the pathways and genes closely related to DVT. Through proteomic analysis, we found that the ferroptosis signaling pathway showed differential expression, and we also discovered that NAT10 (a key acetyltransferase modified by ac4C) was significantly overexpressed in DVT mice. Based on this discovery, we further investigated the downstream genes regulated by NAT10. We found that NAT10 enhances the stability of HMOX1 through ac4C modification, which results in iron overload and lipid peroxides, thereby forming a positive feedback loop that exacerbates DVT.

2026-01-26 | PXD067933 | Pride

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.

2024-07-07 | GSE180494 | GEO

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

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 NaCNBH3-based chemical ac4C sequencing (ac4C-seq).

2023-08-25 | GSE226747 | GEO

ac4C-seq in NAT10-knockdown PANC-1 cells

Project description:Pancreatic cancer is a lethal diease with high tendency of metastasis. Howerver, the mechanisms of pancreatic cancer are sitill unclear. To explore the roles of N4-acetylation (ac4C) RNA modification and its involved N-Acetyltransferase 10 (NAT10) in pancreatic ductal adenocarcinoma (PDAC), we performed profiling by high throughput sequencing. In this study, we investigate the effects of NAT10 knockdown on N4-acetylcytidine (ac4C) modification in mRNA within PANC-1 cells using ac4C-seq. By employing RNA interference to specifically knock down NAT10 expression in PANC-1 cells, we aim to elucidate its impact on ac4C RNA modifications, which have been implicated in various cellular processes and cancer progression. Total RNA was extracted and mRNA was captured and treated with sodium borohydride (NaBH4) for detection of ac4C sites.Following library preparation, sequencing was performed on an Illumina Novaseq 6000 platform. Bioinformatics analyses identified significant changes in ac4C modification patterns due to NAT10 depletion. This dataset provides a valuable resource for further exploration of ac4C modifications in mRNA and their role in PDAC.

2025-03-26 | GSE275963 | GEO

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