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NAT10 is identified as a novel driver for brain metastasis

ABSTRACT: NAT10 is identified as a novel driver for brain metastasis

PROVIDER: PRJNA1120428 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29295856_1.fastq.gz	Fastqsanger.gz
	SRR29295856_2.fastq.gz	Fastqsanger.gz

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NAT10 is identified as a novel driver for brain metastasis

Project description:Metastatic breast cancer remains a major cause of cancer related deaths in women and there are few effective therapies against this advanced disease. Using in vivo and in vitro genetic screens, we identified NAT10 as a driver for breast cancer brain metastassis. Here, we profile the transcriptome of metastatic breast cancer cells MDA-MB-231-BrM3 following NAT10 knockdown, aiming to identify the downstream effectors of NAT10.

2024-11-24 | GSE269160 | GEO

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

Function and Mechanism of NAT10-mediated N4-acetylcytidine modification in osteosarcoma [RIP-seq]

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.

2024-08-09 | GSE237840 | GEO

Function and Mechanism of NAT10-mediated N4-acetylcytidine modification in osteosarcoma [mRNA-seq]

2024-08-09 | GSE237541 | GEO

NAT10 inhibition improves cellular phenotypes of Hutchinson-Gilford progeria syndrome by restoring the Transportin-1 pathway

Project description:In this experiment, we aim to examine the role of NAT10 inhibition in Hutchinson-Gilford progeria syndrome (HGPS), a rare but devastating premature ageing syndrome caused by a mutation in the LMNA gene. NAT10 inhibition improves HGPS cellular phenotypes by releasing Transportin-1 (TNPO1) from the cytoplasm, restoring the TNPO1 pathway and allowing hnRNPA1 and NUP153 nuclear import, TPR anchorage at the nuclear pore complexes and RanGTP gradient re-balancing. We have promoted NAT10 inhibition by two ways in normal or patient derived primary skin fibroblasts; the NAT10 inhibitor Remodelin, and an siRNA directly targeting NAT10 (siNAT10). In addition, we have also used an siRNA against TNPO1 and a combined siTNPO1 and siNAT10 treatment. This is a 2-factor design, with treatment (Remodelin vs untreated, or siNAT10 vs siCT) and condition (HGPS vs normal fibroblasts) as the two conditions. Transcriptional profiling was performed using HumanHT-12 v4 Expression BeadChip microarrays, and all conditions were run in triplicate.

2018-06-25 | E-MTAB-6651 | biostudies-arrayexpress

NSD2 is an actionable driver of prostate cancer metastasis

Project description:NSD2 is an actionable driver of prostate cancer metastasis

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Targeting NAT10 enhances healthspan and lifespan in a mouse model of human accelerated aging syndrome.

Project description:Targeting NAT10 enhances healthspan and lifespan in a mouse model of human accelerated aging syndrome.

2018-03-22 | E-MTAB-6578 | biostudies-arrayexpress

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

2022-08-03 | GSE210017 | GEO

N-acetyltransferase NAT10 Controls Cell Fates

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

NAT10-ac4C axis promote renal fibrosis

Project description:RNA modification play vital roles in renal fibrosis. However, whether ac4C modification functions in renal fibrogenesis remains unknown. Here, we found that NAT10-ac4C axis plays pro—fibrotic role in kidney. ac4C RIP sequencing demonstrated NAT10-ac4C axis functions via regulating multiple master genes of exosome secretion in tubular epithelial cells. In summary, targeting NAT10-ac4C axis is a promising strategy for renal fibrosis.

2024-11-30 | GSE248203 | GEO

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