ArticleOncotarget2017
NatB-mediated protein N-α-terminal acetylation is a potential therapeutic target in hepatocellular carcinoma.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 32 citations in OpenAlex.
- Structural basis of cotranslational protein N-terminal acetylation by NatB in human cells.Nature communications · 2026Article
- 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
- Sequential CRISPR screening reveals partial NatB inhibition as a strategy to mitigate alpha-synuclein levels in human neurons.Science advances · 2024Article
- NatB Protects Procaspase-8 from UBR4-Mediated Degradation and Is Required for Full Induction of the Extrinsic Apoptosis Pathway.Molecular and cellular biology · 2024Article
- Impact of Protein NLife (Basel, Switzerland) · 2023Review
- NatB Catalytic Subunit Depletion Disrupts DNA Replication Initiation Leading to Senescence in MEFs.International journal of molecular sciences · 2023Article
- NAA60 (HAT4): the newly discovered bi-functional Golgi member of the acetyltransferase family.Clinical epigenetics · 2022Review
- From Nucleus to Membrane: A Subcellular Map of the N-Acetylation Machinery in Plants.International journal of molecular sciences · 2022Review
- How important is the N-terminal acetylation of alpha-synuclein for its function and aggregation into amyloids?Frontiers in neuroscience · 2022Review
- Advances in prognostic and therapeutic targets for hepatocellular carcinoma and intrahepatic cholangiocarcinoma: The hippo signaling pathway.Frontiers in oncology · 2022Review
- Structural basis of Naa20 activity towards a canonical NatB substrate.Communications biology · 2021Article
- Identification of NAA40 as a Potential Prognostic Marker for Aggressive Liver Cancer Subtypes.Frontiers in oncology · 2021Article
- NAA10 as a New Prognostic Marker for Cancer Progression.International journal of molecular sciences · 2020Review
- N-Terminal Acetyltransferases Are Cancer-Essential Genes Prevalently Upregulated in Tumours.Cancers · 2020Article
- Article
- NatB regulates Rb mutant cell death and tumor growth by modulating EGFR/MAPK signaling through the N-end rule pathways.PLoS genetics · 2020Article
- Co-translational, Post-translational, and Non-catalytic Roles of N-Terminal Acetyltransferases.Molecular cell · 2019Review
- Spotlight on protein N-terminal acetylation.Experimental & molecular medicine · 2018Review
- Structure of Human NatA and Its Regulation by the Huntingtin Interacting Protein HYPK.Structure (London, England : 1993) · 2018Article
Corrections and comments
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Authors and funding
13 authors at 7 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The identification of new targets for systemic therapy of hepatocellular carcinoma (HCC) is an urgent medical need. Recently, we showed that hNatB catalyzes the N-α-terminal acetylation of 15% of the human proteome and that this action is necessary for proper actin cytoskeleton structure and function. In tumors, cytoskeletal changes influence motility, invasion, survival, cell growth and tumor progression, making the cytoskeleton a very attractive antitumor target. Here, we show that hNatB subunits are upregulated in in over 59% HCC tumors compared to non-tumor tissue and that this upregulation is associated with microscopic vascular invasion. We found that hNatB silencing blocks proliferation and tumor formation in HCC cell lines in association with hampered DNA synthesis and impaired progression through the S and the G2/M phases. Growth inhibition is mediated by the degradation of two hNatB substrates, tropomyosin and CDK2, which occurs when these proteins lack N-α-terminal acetylation. In addition, hNatB inhibition disrupts the actin cytoskeleton, focal adhesions and tight/adherens junctions, abrogating two proliferative signaling pathways, Hippo/YAP and ERK1/2. Therefore, inhibition of NatB activity represents an interesting new approach to treating HCC by blocking cell proliferation and disrupting actin cytoskeleton 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.