ArticleApoptosis : an international journal on programmed cell death2016
Depletion of histone N-terminal-acetyltransferase Naa40 induces p53-independent apoptosis in colorectal cancer cells via the mitochondrial pathway.
Article in Apoptosis : an international journal on programmed cell death, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.
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35 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.
- Histone and Histone Acetylation-Related Alterations of Gene Expression in Uninvolved Psoriatic Skin and Their Effects on Cell Proliferation, Differentiation, and Immune Responses.International journal of molecular sciences · 2023Pooled it
- NatD promotes glioblastoma progression through epigenetic activation of FGFR4 signalling.Experimental & molecular medicine · 2026Article
- A Cell-Potent Bisubstrate Inhibitor to Probe NatD Acetyltransferase Activity.ACS chemical biology · 2025Article
- H2A.X N-terminal acetylation is a newly identified NAA40-mediated modification that is responsive to UV irradiation.Epigenetics & chromatin · 2025Article
- RNF112, whose transcription is regulated by KLF4, inhibits colorectal cancer growth via promoting ubiquitin-dependent degradation of NAA40.Cell biology and toxicology · 2025Article
- Purification and activity assays of N-terminal acetyltransferase D.Methods in enzymology · 2025Article
- Gene Expression Regulation and the Signal Transduction of Programmed Cell Death.Current issues in molecular biology · 2024Review
- N(alpha)-acetyltransferase 40-mediated histone acetylation plays an important role in ecdysone regulation of metamorphosis in the red flour beetle, Tribolium castaneum.Communications biology · 2024Article
- PPARα Agonism Enhances Immune Response to Radiotherapy While Dietary Oleic Acid Results in Counteraction.Clinical cancer research : an official journal of the American Association for Cancer Research · 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
- From Nucleus to Membrane: A Subcellular Map of the N-Acetylation Machinery in Plants.International journal of molecular sciences · 2022Review
- Article
- The role of protein acetylation in carcinogenesis and targeted drug discovery.Frontiers in endocrinology · 2022Review
- Effects of Estrogen on Cardiac mRNA and LncRNA Expression Profiles in Hypertensive Mice.Journal of cardiovascular translational research · 2021Article
- Novel Bisubstrate Inhibitors for Protein N-Terminal Acetyltransferase D.Journal of medicinal chemistry · 2021Article
- N-Terminal Acetyltransferase Naa40p Whereabouts Put into N-Terminal Proteoform Perspective.International journal of molecular sciences · 2021Article
- Development of A Continuous Fluorescence-Based Assay forInternational journal of molecular sciences · 2021Article
- Identification of NAA40 as a Potential Prognostic Marker for Aggressive Liver Cancer Subtypes.Frontiers in oncology · 2021Article
- Classification and phylogeny for the annotation of novel eukaryotic GNAT acetyltransferases.PLoS computational biology · 2020Article
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Abstract
Protein N-terminal acetylation is an abundant post-translational modification in eukaryotes implicated in various fundamental cellular and biochemical processes. This modification is catalysed by evolutionarily conserved N-terminal acetyltransferases (NATs) whose deregulation has been linked to cancer development and thus, are emerging as useful diagnostic and therapeutic targets. Naa40 is a highly selective NAT that acetylates the amino-termini of histones H4 and H2A and acts as a sensor of cell growth in yeast. In the present study, we examine the role of Naa40 in cancer cell survival. We demonstrate that depletion of Naa40 in HCT116 and HT-29 colorectal cancer cells decreases cell survival by enhancing apoptosis, whereas Naa40 reduction in non-cancerous mouse embryonic fibroblasts has no effect on cell viability. Specifically, Naa40 knockdown in colon cancer cells activates the mitochondrial caspase-9-mediated apoptotic cascade. Consistent with this, we show that caspase-9 activation is required for the induced apoptosis because treatment of cells with an irreversible caspase-9 inhibitor impedes apoptosis when Naa40 is depleted. Furthermore, the effect of Naa40-depletion on cell-death is mediated through a p53-independent mechanism since p53-null HCT116 cells still undergo apoptosis upon reduction of the acetyltransferase. Altogether, these findings reveal an anti-apoptotic role for Naa40 and exhibit its potential as a therapeutic target in colorectal cancers.
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