ArticleThe Journal of clinical investigation2010
hNaa10p contributes to tumorigenesis by facilitating DNMT1-mediated tumor suppressor gene silencing.
Article in The Journal of clinical investigation, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.
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Who cites it
66 citing papers in PubMed, 115 citations in OpenAlex.
- N-terminal modifications as fate switches in neurodegeneration: a mechanistic review.Frontiers in aging neuroscience · 2026Review
- HYPK promotes N-terminal protein acetylation through rapid ribosome exchange of NatA.Molecular cell · 2025Article
- LRRC75A-AS1 facilitates breast cancer cell proliferation and invasion via functioning as a CeRNA to modulate miR489-3p/ARD1.Scientific reports · 2025Article
- NAA10 (N-Alpha-Acetyltransferase 10): A Multifunctional Regulator in Development, Disease, and Cancer.Cells · 2025Review
- Molecular Mechanisms of ARD1 in Tumors.Cancer medicine · 2025Review
- Illuminating the impact of N-terminal acetylation: from protein to physiology.Nature communications · 2025Review
- A repository of Ogden syndrome patient derived iPSC lines and isogenic pairs by X-chromosome screening and genome-editing.bioRxiv : the preprint server for biology · 2024Article
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- Naa10p promotes cell invasiveness of esophageal cancer by coordinating the c-Myc and PAI1 regulatory axis.Cell death & disease · 2022Article
- From Nucleus to Membrane: A Subcellular Map of the N-Acetylation Machinery in Plants.International journal of molecular sciences · 2022Review
- Epigenetic signature of N-terminal acetyltransferases: a probable mediator of immune and neuropathogenesis in HIV infection.Molecular brain · 2022Review
- Biochemical analysis of novel NAA10 variants suggests distinct pathogenic mechanisms involving impaired protein N-terminal acetylation.Human genetics · 2022Article
- N-α-Acetyltransferase 10 inhibits invasion and metastasis of oral squamous cell carcinoma via regulating Pirh2-p53 signalling pathway.Journal of cellular and molecular medicine · 2022Article
- High Maternal Serum Estradiol in First Trimester of Multiple Pregnancy Contributes to Small for Gestational Age via DNMT1-Mediated CDKN1C Upregulation.Reproductive sciences (Thousand Oaks, Calif.) · 2022Article
- Hydroxylation of the Acetyltransferase NAA10 Trp38 Is Not an Enzyme-Switch in Human Cells.International journal of molecular sciences · 2021Article
- Clinical Manifestations in a Girl with NAA10-Related Syndrome and Genotype-Phenotype Correlation in Females.Genes · 2021Article
- Overlap of NatA and IAP substrates implicates N-terminal acetylation in protein stabilization.Science advances · 2021Article
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- NAA10 as a New Prognostic Marker for Cancer Progression.International journal of molecular sciences · 2020Review
6 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 5 institutions in 2 countries.
Funding
Abstract
Hypermethylation-mediated tumor suppressor gene silencing plays a crucial role in tumorigenesis. Understanding its underlying mechanism is essential for cancer treatment. Previous studies on human N-alpha-acetyltransferase 10, NatA catalytic subunit (hNaa10p; also known as human arrest-defective 1 [hARD1]), have generated conflicting results with regard to its role in tumorigenesis. Here we provide multiple lines of evidence indicating that it is oncogenic. We have shown that hNaa10p overexpression correlated with poor survival of human lung cancer patients. In vitro, enforced expression of hNaa10p was sufficient to cause cellular transformation, and siRNA-mediated depletion of hNaa10p impaired cancer cell proliferation in colony assays and xenograft studies. The oncogenic potential of hNaa10p depended on its interaction with DNA methyltransferase 1 (DNMT1). Mechanistically, hNaa10p positively regulated DNMT1 enzymatic activity by facilitating its binding to DNA in vitro and its recruitment to promoters of tumor suppressor genes, such as E-cadherin, in vivo. Consistent with this, interaction between hNaa10p and DNMT1 was required for E-cadherin silencing through promoter CpG methylation, and E-cadherin repression contributed to the oncogenic effects of hNaa10p. Together, our data not only establish hNaa10p as an oncoprotein, but also reveal that it contributes to oncogenesis through modulation of DNMT1 function.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.