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

ABSTRACT: 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

ORGANISM(S): Homo sapiens

PROVIDER: GSE231762 | GEO | 2023/05/10

REPOSITORIES: GEO

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Microarray expression profile of circular RNAs in cervical cancer

Project description:Human immortal cervical cell line H8, human cervical cancer cell line SiHa and SiHa transfected with Wnt11-overexpression vector were included in the study. We identified circRNAs differentially expressed between H8 and SiHa or between SiHa and SiHa transfected with OV-Wnt11.

2020-03-25 | GSE147483 | GEO

Acetylation of cytidines by NAT10 enhances HIV-1 replication through stabilization of viral RNA

Project description:As obligate parasites, viruses need to navigate a variety of cellular regulatory systems while infecting and replicating in the host cell. Post-transcriptional modifications have recently emerged as an important layer of regulation of viral RNA function. For example, our lab and others have shown that the RNA modification N6-methyladenosine (m6A) can enhance the replication of multiple viruses in cis, including Human Immunodeficiency virus 1 (HIV-1), Influenza A virus, SV40 and Kaposi's sarcoma-associated herpesvirus (KSHV). Recent reports have revealed the presence of another RNA modification, N4-acetylcytidine (ac4C) on cellular mRNAs and have shown that ac4C can enhance mRNA stability and translation. Here, we demonstrate that ac4C is present at multiple sites on HIV-1 mRNAs and on the viral genomic RNA. Through ac4C RNA immunoprecipitation (RNA-IP) and RNA-seq, we found ac4C on HIV-1 mRNAs as well as the virion genomic RNA, with ac4C sites in the coding regions of the pol, env, nef genes, and the trans-activation response (TAR) hairpin. Phenotypically, we observe that increasing the expression level of the ac4C acetyltransferase NAT10 leads to an increase in viral replication that is dependent on the RNA binding and enzymatic domains of NAT10. Moreover, both CRISPR-depletion of NAT10 (ΔNAT10) and treatment with the small molecule NAT10 inhibitor Remodelin, diminishes HIV-1 replication in T cells. Lastly, silent mutations introduced to prevent ac4C deposition on the viral genome indeed diminished HIV-1 replication. Our data suggest that HIV-1 has evolved to incorporate ac4C in essential viral gene coding regions and regulatory RNA structures, and that NAT10-dependent ac4C addition enhances HIV-1 replication.

2020-06-11 | GSE142490 | 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.

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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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Knock down of FTO in cervical cancer cells

Project description:FTO, an N6-methyladenosine (m6A) demethylase, can promote cervical cancer cell proliferation and migration. RNA-sequencing of SiHa cells with FTO knockdown was conducted to dissect the differentially expressed genes and the potential mechanism of FTO in cervical cancer.

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The acRIP-seq of SiHa and KONAT10SiHa cells

Project description:We investigate genes that the different degrees of N4-acetylcytidine in the SiHa and Knockout NAT10 SiHa.

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Microarray expression profile and functional analysis of circular RNAs in cervical cancer

Project description:Five human cervical cancer cell lines (HeLa, CaSki, SiHa, C-33A, SW756) and one human normal cervical epithelial cell line HcerEpic were included in the study. Microarray based circRNA expression profiles were acquired using the Arraystar Human circRNA Array (8x15K, Arraystar). We identified circRNAs differentially expressed in human cervical cancer cell lines compared to human normal cervical epithelial HcerEpic cells (control).

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NAT10-mediated mRNA N4-acetylation is Essential for the Translational Regulation During Oocyte Meiotic Maturation in Mice

Project description:Mammalian oocyte maturation is driven by strictly translational regulation of maternal mRNAs stored in the cytoplasm. However, the function and mechanism of post-transcriptional chemical modifications especially the newly identified N4-acetylcytidine (ac4C) catalyzed by N-acetyltransferase 10 (NAT10) in this process are previously unknown. In this study, we developed a low-input ac4C sequencing technology—ac4C LACE-seq and mapped 8241 ac4C peaks at the whole transcriptome level using 50 mouse oocytes at the germinal vesicle (GV) stage. We profiled the mRNA landscapes of NAT10-interactions and ac4C modifications. The NAT10-interacted and ac4C modified transcripts displayed association with high translation efficiency in oocytes. Oocyte-specific Nat10 knockout wiped out ac4C signals in oocytes and caused severe defects in meiotic maturation and female infertility. ac4C LACE-seq results indicated that Nat10 deletion led to a failure of ac4C deposition on mRNAs encoding key maternal factors such as MAY2, ZAR1, BTG4 and cyclin B1 that regulate transcriptome stability and maternal-to-zygotic transition. Nat10-deleted oocytes had decreased mRNA translation efficiencies during meiotic maturation, partially due to the direct inhibition ac4C sites on specific transcripts. In sum, we developed low-input, high-sensitivity mRNA ac4C profiling approach and highlighted the important physiological function of ac4C in precise regulation of the oocyte meiotic maturation by enhancing translation efficiency.

2024-02-18 | GSE254288 | 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

ChIP-Seq hnRNP E1, Cervical cancer SiHa cells

Project description:Based on the specificity with which the unique KH structural domains of hnRNP E1 bind with RNA/DNA, considering that HPV16 provides RNA/DNA binding sites, we hypothesized that hnRNP E1 may be crucial to HPV16 oncogenes expression and cervical carcinogenesis. Based on the main purpose of this study was to explore the role of hnRNP E1 on the regulation of HPV16 oncogene expression in cervical cancerization, we conducted ChIP-seq in the untreated SiHa cell line.

2022-06-16 | GSE203023 | GEO

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