ArticleFrontiers in oncology2021
Identification of NAA40 as a Potential Prognostic Marker for Aggressive Liver Cancer Subtypes.
Article in Frontiers in oncology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- NatD promotes glioblastoma progression through epigenetic activation of FGFR4 signalling.Experimental & molecular medicine · 2026Article
- Mechanism of cotranslational modification of histones H2A and H4 by MetAP1 and NatD.Science advances · 2025Article
- Illuminating the impact of N-terminal acetylation: from protein to physiology.Nature communications · 2025Review
- Purification and activity assays of N-terminal acetyltransferase D.Methods in enzymology · 2025Article
- TREM1 is essential for maintaining stemness of liver cancer stem-like cells in hepatocellular carcinoma.Frontiers in immunology · 2025Article
- Biochemical Characterisation of the Short Isoform of Histone N-Terminal Acetyltransferase NAA40.Biomolecules · 2024Article
- NatD epigenetically activates FOXA2 expression to promote breast cancer progression by facilitating MMP14 expression.iScience · 2024Article
- Exploring the role of NAA40 in immune infiltrates and prognostic prediction in hepatocellular carcinoma.American journal of clinical and experimental immunology · 2024Article
- Article
- Pan-cancer analysis reveals NAA50 as a cancer prognosis and immune infiltration-related biomarker.Frontiers in genetics · 2022Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Liver hepatocellular carcinoma (LIHC) is a leading cause of cancer-related mortality. In this study we initially interrogated the Cancer Genome Atlas (TCGA) dataset to determine the implication of N-terminal acetyltransferases (NATs), a family of enzymes that modify the N-terminus of the majority of eukaryotic proteins, in LIHC. This examination unveiled NAA40 as the NAT family member with the most prominent upregulation and significant disease prognosis for this cancer. Focusing on this enzyme, which selectively targets histone proteins, we show that its upregulation occurs from early stages of LIHC and is not specifically correlated with any established risk factors such as viral infection, obesity or alcoholic disease. Notably, in silico analysis of TCGA and other LIHC datasets found that expression of this epigenetic enzyme is associated with high proliferating, poorly differentiating and more aggressive LIHC subtypes. In particular, NAA40 upregulation was preferentially linked to mutational or non-mutational P53 functional inactivation. Accordingly, we observed that high NAA40 expression was associated with worse survival specifically in liver cancer patients with inactivated P53. These findings define NAA40 as a NAT with potentially oncogenic functions in LIHC and uncover its prognostic value for aggressive LIHC subtypes.
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