ArticleCancer medicine2019
MYST1/KAT8 contributes to tumor progression by activating EGFR signaling in glioblastoma cells.
Article in Cancer medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
19 citing papers in PubMed, 32 citations in OpenAlex.
- KAT8-mediated epigenetic modifications: Physiological functions, heterogeneity in disease, and advances in targeted development.iScience · 2026Review
- Article
- Lysine Acetyltransferase 8: A Target for Natural Compounds in Cancer Therapy.International journal of molecular sciences · 2025Review
- Immunogenic profiling of metastatic uveal melanoma discerns a potential signature related to prognosis.Journal of cancer research and clinical oncology · 2024Article
- Expression profiles and functional prediction of histone acetyltransferases of the MYST family in kidney renal clear cell carcinoma.BMC cancer · 2023Article
- KAT8 acetylation-controlled lipolysis affects the invasive and migratory potential of colorectal cancer cells.Cell death & disease · 2023Article
- NAA60 (HAT4): the newly discovered bi-functional Golgi member of the acetyltransferase family.Clinical epigenetics · 2022Review
- Histone acetylation modification regulator-mediated tumor microenvironment infiltration characteristics and prognostic model of lung adenocarcinoma patients.Journal of thoracic disease · 2022Article
- Article
- The role of protein acetylation in carcinogenesis and targeted drug discovery.Frontiers in endocrinology · 2022Review
- Role of the Histone Acetyl Transferase MOF and the Histone Deacetylase Sirtuins in Regulation of H4K16ac During DNA Damage Repair and Metabolic Programming: Implications in Cancer and Aging.Sub-cellular biochemistry · 2022Article
- Lysine Acetyltransferases and Their Role in AR Signaling and Prostate Cancer.Frontiers in endocrinology · 2022Review
- Interplay between Epigenetics and Cellular Metabolism in Colorectal Cancer.Biomolecules · 2021Review
- KAT8, lysine acetyltransferase 8, is required for adipocyte differentiation in vitro.Biochimica et biophysica acta. Molecular basis of disease · 2021Article
- Protein Acetylation at the Interface of Genetics, Epigenetics and Environment in Cancer.Metabolites · 2021Review
- Acetylation Profiles in the Metabolic Process of Glioma-Associated Seizures.Frontiers in neurology · 2021Article
- Lysine Acetylation in the Proteome of Renal Tubular Epithelial Cells in Diabetic Nephropathy.Frontiers in genetics · 2021Article
- Gene co-expression and histone modification signatures are associated with melanoma progression, epithelial-to-mesenchymal transition, and metastasis.Clinical epigenetics · 2020Article
- MYST1/KAT8 contributes to tumor progression by activating EGFR signaling in glioblastoma cells.Cancer medicine · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
With short survival time, glioblastoma (GBM) is the most malignant tumor in the central nervous system. Recently, epigenetic enzymes play essential roles in the regulation of tumorigenesis and cancer development of GBM. However, little is known about MYST1/KAT8/MOF, a histone acetylation enzyme, in GBM. The present study shows that MYST1 promotes GBM progression through activating epidermal growth factor receptor (EGFR) signaling. MYST1 expression was increased in GBM and was negatively correlated with prognosis in patients with glioma and GBM. Knockdown of MYST1 reduced cell proliferation and BrdU incorporation in LN229, U87, and A172 GBM cells. Besides, MYST1 downregulation also induced cell cycle arrest at G2M phase, as well as the reduced expression of CDK1, Cyclin A, Cyclin B1, and increased expression of p21
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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.