Unmasking the biological function and regulatory mechanism of NOC2L: a novel inhibitor of histone acetyltransferase

Lu, Siyi; Chen, Zhaoyu; Liu, Zhenzhen; Liu, Zhentao

doi:10.1186/s12967-023-03877-2

Cited by 7 publications

(4 citation statements)

References 72 publications

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“…Histones H1x and H1.0 are linker histones and are classified as strong condensers of chromatin structure [19]. Nucleolar complex protein 2 homolog (NOC2L) is an inhibitor of histone acetyltransferase [20]. UHRF1 is a key regulator of CpG methylation [21–23].…”

Section: Resultsmentioning

confidence: 99%

iChIP‐SILAC analysis identifies epigenetic regulators of CpG methylation of the p16^INK4A gene

Fujita,

Fujii

2024

FEBS Letters

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Allele‐specific epigenetic events regulate the expression of specific genes such as tumor suppressor genes. Methods to biochemically identify epigenetic regulators remain limited. Here, we used insertional chromatin immunoprecipitation (iChIP) to address this issue. iChIP combined with quantitative mass spectrometry identified DNA methyltransferase 1 (DNMT1) and epigenetic regulators as proteins that potentially interact with a region of the p16INK4A gene that is CpG‐methylated in one allele in HCT116 cells. Some of the identified proteins are involved in the CpG methylation of this region, and of these, DEAD‐box helicase 24 (DDX24) contributes to CpG methylation by regulating the protein levels of DNMT1. Thus, iChIP is a useful method to identify proteins which bind to a target locus of interest.

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Section: Resultsmentioning

confidence: 99%

iChIP‐SILAC analysis identifies epigenetic regulators of CpG methylation of the p16^INK4A gene

Fujita,

Fujii

2024

FEBS Letters

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“…NOC2L, also known as NIR, is involved in cell proliferation and apoptosis [ 15 ]. One possible explanation for its effect on cell proliferation is that NOC2L acts as a suppressor of p53, thereby reversing the detrimental impact of p53 overexpression on embryonic development [ 27 ]. Our results also confirmed that overexpression of NOC2L could enhance cell proliferation and reduce apoptosis in trophoblasts.…”

Section: Discussionmentioning

confidence: 99%

Preeclampsia-associated lncRNA FEZF1-AS1 regulates cell proliferation and apoptosis in placental trophoblast cells through the ELAVL1/NOC2L axis

Zhao,

Su,

Guo

et al. 2023

Cell Div

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Background LncRNAs have been shown to be involved in and control the biological processes of multiple diseases, including preeclampsia (PE). The impairment of trophoblast cell proliferation is recognized as a significant anomaly contributing to the development of PE. LncRNA FEZF1-AS1 was found downregulated in placental tissues of PE patients. However, the precise regulatory mechanism of FEZF1-AS1 in placental trophoblast proliferation and apoptosis remains unclear. Results In this study, we conducted an investigation into the expression levels of FEZF1-AS1 and NOC2L in placental tissues obtained from patients diagnosed with PE. Subsequently, we employed CCK-8 and EdU assays to quantify cell proliferation, while TUNEL staining and western blot for apoptosis-related protein detection to assess apoptosis. Furthermore, the interactions between FEZF1-AS1 and ELAVL1, as well as NOC2L and ELAVL1, were confirmed through the implementation of RIP and RNA pull-down assays. We found a downregulation of lncRNA FEZF1-AS1 and NOC2L in placental tissues of PE patients. Overexpression of FEZF1-AS1 or NOC2L resulted in increased cell proliferation and inhibition of apoptosis, whereas knockdown of FEZF1-AS1 or NOC2L had the opposite effect. In addition, lncRNA FEZF1-AS1 stabilized NOC2L mRNA expression by interacting with ELAVL1. Moreover, partial reversal of the effects of FEZF1-AS1 overexpression on cell proliferation and apoptosis was observed upon suppression of ELAVL1 or NOC2L. Conclusions PE related lncRNA FEZF1-AS1 could regulate apoptosis and proliferation of placental trophoblast cells through the ELAVL1/NOC2L axis.

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“…Examples of EV RNA sequences that are exclusive to all NCD samples include miR-12136, a regulator of translation (68), NOC2L, a regulator of histone acetyltransferase activity (69) and PERM1, a regulator of mitochondrial content and oxidative function (70). In addition, lncRNA LINC01134 directly binds the promoter of AKTISI, which in turn leading to activation of the NFKB signaling pathway (71).…”

Section: Discussionmentioning

confidence: 99%

Extracellular vesicle small RNA cargo discriminates non-cancer donors from pediatric B-lymphoblastic leukemia patients

Longjohn,

Hudson,

Peña-Castillo

et al. 2023

Front. Oncol.

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Pediatric B-acute lymphoblastic leukemia (B-ALL) is a disease of abnormally growing B lymphoblasts. Here we hypothesized that extracellular vesicles (EVs), which are nanosized particles released by all cells (including cancer cells), could be used to monitor B-ALL severity and progression by sampling plasma instead of bone marrow. EVs are especially attractive as they are present throughout the circulation regardless of the location of the originating cell. First, we used nanoparticle tracking analysis to compare EVs between non-cancer donor (NCD) and B-ALL blood plasma; we found that B-ALL plasma contains more EVs than NCD plasma. We then isolated EVs from NCD and pediatric B-ALL peripheral blood plasma using a synthetic peptide-based isolation technique (Vn96), which is clinically amenable and isolates a broad spectrum of EVs. RNA-seq analysis of small RNAs contained within the isolated EVs revealed a signature of differentially packaged and exclusively packaged RNAs that distinguish NCD from B-ALL. The plasma EVs contain a heterogenous mixture of miRNAs and fragments of long non-coding RNA (lncRNA) and messenger RNA (mRNA). Transcripts packaged in B-ALL EVs include those involved in negative cell cycle regulation, potentially suggesting that B-ALL cells may use EVs to discard gene sequences that control growth. In contrast, NCD EVs carry sequences representative of multiple organs, including brain, muscle, and epithelial cells. This signature could potentially be used to monitor B-ALL disease burden in pediatric B-ALL patients via blood draws instead of invasive bone marrow aspirates.

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Unmasking the biological function and regulatory mechanism of NOC2L: a novel inhibitor of histone acetyltransferase

Cited by 7 publications

References 72 publications

iChIP‐SILAC analysis identifies epigenetic regulators of CpG methylation of the p16^INK4A gene

iChIP‐SILAC analysis identifies epigenetic regulators of CpG methylation of the p16^INK4A gene

Preeclampsia-associated lncRNA FEZF1-AS1 regulates cell proliferation and apoptosis in placental trophoblast cells through the ELAVL1/NOC2L axis

Extracellular vesicle small RNA cargo discriminates non-cancer donors from pediatric B-lymphoblastic leukemia patients

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Unmasking the biological function and regulatory mechanism of NOC2L: a novel inhibitor of histone acetyltransferase

Cited by 7 publications

References 72 publications

iChIP‐SILAC analysis identifies epigenetic regulators of CpG methylation of the p16INK4A gene

iChIP‐SILAC analysis identifies epigenetic regulators of CpG methylation of the p16INK4A gene

Preeclampsia-associated lncRNA FEZF1-AS1 regulates cell proliferation and apoptosis in placental trophoblast cells through the ELAVL1/NOC2L axis

Extracellular vesicle small RNA cargo discriminates non-cancer donors from pediatric B-lymphoblastic leukemia patients

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iChIP‐SILAC analysis identifies epigenetic regulators of CpG methylation of the p16^INK4A gene

iChIP‐SILAC analysis identifies epigenetic regulators of CpG methylation of the p16^INK4A gene