ArticleMolecular cancer2015
Knockdown of NAT12/NAA30 reduces tumorigenic features of glioblastoma-initiating cells.
Article in Molecular cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 38 citations in OpenAlex.
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- Functional mapping of N-terminal residues in the yeast proteome uncovers novel determinants for mitochondrial protein import.PLoS genetics · 2023Article
- Pan-cancer analysis reveals NAA50 as a cancer prognosis and immune infiltration-related biomarker.Frontiers in genetics · 2022Article
- Molecular mechanism of N-terminal acetylation by the ternary NatC complex.Structure (London, England : 1993) · 2021Article
- [Overexpression of lncRNA MEG3 inhibits proliferation and invasion of glioblastoma U251 cellsNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2021Article
- Divergent architecture of the heterotrimeric NatC complex explains N-terminal acetylation of cognate substrates.Nature communications · 2020Article
- 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
- A Small-Molecule Tankyrase Inhibitor Reduces Glioma Stem Cell Proliferation and Sphere Formation.Cancers · 2020Article
- Detailed modeling of positive selection improves detection of cancer driver genes.Nature communications · 2019Article
- Co-translational, Post-translational, and Non-catalytic Roles of N-Terminal Acetyltransferases.Molecular cell · 2019Review
- Phenotypic and Expressional Heterogeneity in the Invasive Glioma Cells.Translational oncology · 2019Article
- Patterns of Invasive Growth in Malignant Gliomas-The Hippocampus Emerges as an Invasion-Spared Brain Region.Neoplasia (New York, N.Y.) · 2018Article
- NatB-mediated protein N-α-terminal acetylation is a potential therapeutic target in hepatocellular carcinoma.Oncotarget · 2017Article
- Post-translational modifications of FDA-approved plasma biomarkers in glioblastoma samples.PloS one · 2017Article
- Brain tissue banking for stem cells for our future.Scientific reports · 2016Article
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGlioblastoma (GBM) is the most common primary brain malignancy and confers a dismal prognosis. GBMs harbor glioblastoma-initiating cells (GICs) that drive tumorigenesis and contribute to therapeutic resistance and tumor recurrence. Consequently, there is a strong rationale to target this cell population in order to develop new molecular therapies against GBM. Accumulating evidence indicates that Nα-terminal acetyltransferases (NATs), that are dysregulated in numerous human cancers, can serve as therapeutic targets.
methodsMicroarrays were used to study the expression of several NATs including NAT12/NAA30 in clinical samples and stem cell cultures. The expression of NAT12/NAA30 was analyzed using qPCR, immunolabeling and western blot. We conducted shRNA-mediated knockdown of NAT12/NAA30 gene in GICs and studied the effects on cell viability, sphere-formation and hypoxia sensitivity. Intracranial transplantation to SCID mice enabled us to investigate the effects of NAT12/NAA30 depletion in vivo. Using microarrays we identified genes and biochemical pathways whose expression was altered upon NAT12/NAA30 down-regulation.
resultsWhile decreased expression of the distal 3'UTR of NAT12/NAA30 was generally observed in GICs and GBMs, this gene was strongly up-regulated at the protein level in GBM and GICs. The increased protein levels were not caused by increased levels of the steady state mRNA but rather by other mechanisms. Also, shorter 3'UTR of NAT12/NAA30 correlated with poor survival in glioma patients. As well, we observed previously not described nuclear localization of this typically cytoplasmic protein. When compared to non-silencing controls, cells featuring NAT12/NAA30 knockdown exhibited reduced cell viability, sphere-forming ability, and mitochondrial hypoxia tolerance. Intracranial transplantation showed that knockdown of NAT12/NAA30 resulted in prolonged animal survival. Microarray analysis of the knockdown cultures showed reduced levels of HIF1α and altered expression of several other genes involved in the hypoxia response. Furthermore, NAT12/NAA30 knockdown correlated with expressional dysregulation of genes involved in the p53 pathway, ribosomal assembly and cell proliferation. Western blot analysis revealed reduction of HIF1α, phospho-MTOR(Ser2448) and higher levels of p53 and GFAP in these cultures.
conclusionNAT12/NAA30 plays an important role in growth and survival of GICs possibly by regulating hypoxia response (HIF1α), levels of p-MTOR (Ser2448) and the p53 pathway.
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