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RNA-seq analysis of human colorectal cancer cells with NAT10 deficiency.

ABSTRACT: Transcriptional analysis of DLD-1 and SW480 cells with NAT10 knockdown.

ORGANISM(S): Homo sapiens

PROVIDER: GSE210384 | GEO | 2022/12/27

REPOSITORIES: GEO

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Identification of NAT10 targets in CRC by RNA immunoprecipitation and acethyl-RNA immunoprecipitation

Project description:To identify potential mRNAs that are acetylated by NAT10, RIP with a NAT10 antibody and acRIP with a ac4C antibody were conducted in DLD-1 and SW480 cells

2022-12-27 | GSE210385 | GEO

acRIP-seq to identify NAT10 mediates mRNA ac4C modification in colorectal cancer

Project description:We performedacRIP-seq between control CRC cells and CRC cells with NAT10 knockdown to identify NAT10 mediates mRNA ac4C modification

2022-08-19 | GSE202826 | GEO

RNA-seq analysis of human colorectal cancer cells with NAT10 deficiency.

Project description:RNA-seq analysis of human colorectal cancer cells with NAT10 deficiency.

| PRJNA865553 | ENA

NAT10-mediated RNA acetylation enhances HNRNPUL1 mRNA stability to contribute cervical cancer progression

Project description:To investigate the principal mechanism of NAT10 in cervical cancer, RNA-seq was accomplished in SiHa and Hela cells with NAT10 knockdown and in control cells

2023-05-10 | GSE231762 | GEO

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

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

Transcriptomic 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 determine the impact of NAT10-mediated ac4C on gene expression, we conducted high throughput RNA-sequencing (RNA-seq) in NAT10-knockdown and control MOLM13 cells.

2024-08-26 | GSE246503 | GEO

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

RNA-seq analysis of mRNA expression profiles upon NAT10 depletion

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.

2024-06-30 | GSE180422 | 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

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