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Gene expression changes in NAT10-knockdown primary human endometrial stromal cells (hESCs) compared to control cells

ABSTRACT: To portray the molecular mechanism for NAT10 function in hESCs, cell treated with siNAT10 and siNC were subjected to RNA-seq analysis.

ORGANISM(S): Homo sapiens

PROVIDER: GSE293343 | GEO | 2025/04/15

REPOSITORIES: GEO

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Gene expression changes in UBE2I-knockdown primary human endometrial stromal cells (hESCs) compared to control cells

Project description:To portray the molecular mechanism for UBE2I function in hESCs, cell treated with siUBE2I and siNC were subjected to RNA-seq analysis.

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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

Gene expression changes in NAT10-knockdown primary human endometrial stromal cells (hESCs) compared to control cells

Project description:Gene expression changes in NAT10-knockdown primary human endometrial stromal cells (hESCs) compared to control cells

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Gene expression changes in Nat10-deleted mouse uterus on PND21

Project description:We specifically deleted Nat10 in the female reproductive tract using the Pgr-Cre driver. To portray the molecular mechanism for Nat10 function in uterus, uterine tissues were collected from Nat10f/f and Nat10d/d mice on PND21 and subjected to RNA-seq analysis.

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N-acetyltransferase NAT10 Controls Cell Fates via RNA Cytidine Acetylation

Project description:We show that NAT10-ac4C axis significantly regulates cell fates. To identify the molecular mechanisms of NAT10-ac4C-ANP32B axis in cell-fate transitions, we construct shNAT10 and shANP32B hESCs. acRIP-seq of shCTR and shNAT10 hESCs. We profiled ATAC-seq in shCTR, shNAT10, and shANP32B hESCs. We profiled H3K4me3 and H3K27me3 modifications and the binding of ANP32B by CUT&Tag in shCTR and shNAT10 hESCs.

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Gene expression profiling of NAT10 knockdown in HepG2 hepatocellular carcinoma cells by QuantSeq 3' mRNA-seq

Project description:NAT10 (N-acetyltransferase 10) is an RNA acetyltransferase that catalyzes N4-acetylcytidine (ac4C) modification of mRNA and rRNA. To investigate the transcriptomic consequences of NAT10 depletion, we performed siRNA-mediated knockdown of NAT10 in HepG2 hepatocellular carcinoma cells. Total RNA was extracted using TRI reagent 2 days after siRNA transfection, and 3' mRNA-seq libraries were prepared using the Lexogen QuantSeq 3' mRNA-Seq Library Prep Kit FWD. Sequencing was performed on Illumina NovaSeq 6000. Four biological replicates per condition were analyzed: samples 1, 2, 5, 6 are negative control siRNA (siCtrl), and samples 3, 4, 7, 8 are siNAT10 knockdown.

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Inhibition of tumor-intrinsic NAT10 enhances antitumor immunity by triggering type I interferon responses via MYC/CDK2/DNMT1 pathway

Project description:Posttranscriptional modifications are deeply involved in cancer progression; however, there remains knowledge gap regarding the function and immune regulatory mechanism of newly discovered mRNA acetylation modification. Here, we discovered an unexpected role of N4-acetylcytidine (ac4C) RNA acetyltransferase NAT10 in reshaping the tumor immune microenvironment. By analyzing patients' data, we found that NAT10 was upregulated in tumor tissues and negatively correlated with immune cell infiltration and overall survival. Loss of tumoral NAT10 significantly stimulated tumor-specific cellular immune responses and suppressed tumor growth. Mechanistically, we identified MYC as a key downstream target of NAT10 via enhancing mRNA stability and translation efficiency. Inhibition of NAT10 blocked the MYC/CDK2/DNMT1 pathway, subsequently enhancing double-stranded RNAs (dsRNA) formation, which triggered type I interferon responses to enhance the in vivo response of tumor specific CD8+ T cells. More importantly, inhibition of NAT10 using either small molecule inhibitor (Remodelin) or PEI/PC7A/siNAT10 nanoparticles combined with PD-1 blockade synergistically enhanced the anti-tumor immune response and repressed tumor progression. Our findings uncovered the crucial role of tumor-intrinsic NAT10 in tumor immune microenvironment, representing a promising target for enhancing cancer immunotherapy.

2025-05-16 | PXD059596 | Pride

NAT10 mediates TLR2 to promote podocyte senescence in adriamycin-induced nephropathy

Project description:N-acetyltransferase 10 (NAT10) is involved in regulating senescence. However, its role in glomerular diseases remains unclear. Therefore, this study aims to investigate the mechanisms by which NAT10 influences senescence and damage in an adriamycin (ADR)-induced nephropathy model. Senescence (p16 and p21) and DNA damage markers (γ-H2AX (ser139)) were assessed in ADR-induced nephropathy. NAT10 function was demonstrated using Remodelin or small interfering RNA (siRNA) interventions. Transcriptome sequencing was conducted to identify key downstream genes and pathways, while coimmunoprecipitation was performed to evaluate the relationship between NAT10 and toll-like receptor 2 (TLR2) expression. TLR2 overexpression or knockdown further validated its regulatory role in senescence. In ADR-treated mice, the expression levels of P53, P21, P16, γ-H2AX(S139) proteins were elevated, while those of WT-1 and nephrin were reduced. This effect was mitigated by Remodelin and siNAT10 administration. Transcriptome sequencing identified TLR2 as a key downstream gene, and coimmunoprecipitation, along with molecular docking models, confirmed its interaction with NAT10. TLR2 overexpression plasmid or siRNA was employed for recovery experiments. Together, the study findings suggest that NAT10 contributes to podocyte senescence and injury via interaction with TLR2. Further, it demonstrates that NAT10 alleviates ADR-induced podocyte senescence by interacting with TLR2, potentially through a P53-P21-dependent mechanism. Thus NAT10 could serve as a novel therapeutic target for treating podocyte senescence and proteinuric glomerulopathies.

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Expression data from human endometrial stromal cells (HESCs) treated with PRP

Project description:In IVF treatment, the effects of intrauterine platelet-rich plasma (PRP) infusion with increasing rate of successful pregnancy have been reported; however, the mechanisms that support embryo implantation remain unclear. In the undifferentiated HESCs, PRP was found to strongly promote the gene expression associated with cell growth, tissue regeneration, proinflammatory response, and antibiotic effects. In decidualized HESCs, PRP was found to attenuate the gene expression involved in cell proliferation and inflammation by inhibiting the expression of PI3K signaling.

2022-09-24 | GSE213873 | GEO

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