ArticleMolecular endocrinology (Baltimore, Md.)2014
Coactivator MYST1 regulates nuclear factor-κB and androgen receptor functions during proliferation of prostate cancer cells.
Article in Molecular endocrinology (Baltimore, Md.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 34 citations in OpenAlex.
- Acetyltransferase MOF Regulates Macrophage Inflammation in Abdominal Aortic Aneurysms.Circulation research · 2026Article
- Unpacking the Tumor Protein D52-like Family: Roles in Intracellular Trafficking and Cancer Progression.Cells · 2026Review
- Lysine Acetyltransferase 8: A Target for Natural Compounds in Cancer Therapy.International journal of molecular sciences · 2025Review
- Gastrodin attenuates rheumatoid arthritis by targeting KAT8 to inhibit the lactylation of H3K9.Frontiers in pharmacology · 2025Article
- Molecular Sentinels: Unveiling the Role of Sirtuins in Prostate Cancer Progression.International journal of molecular sciences · 2024Review
- Androgen Receptor-Interacting Proteins in Prostate Cancer Development and Therapy Resistance.The American journal of pathology · 2024Review
- Lysine Acetyltransferases and Their Role in AR Signaling and Prostate Cancer.Frontiers in endocrinology · 2022Review
- MOF negatively regulates estrogen receptor α signalingFrontiers in oncology · 2022Article
- Epigenetic Coregulation of Androgen Receptor Signaling.Advances in experimental medicine and biology · 2022Article
- Inflammation induced by lipopolysaccharide advanced androgen receptor expression and epithelial-mesenchymal transition progress in prostatitis and prostate cancer.Translational andrology and urology · 2021Article
- Deacetylation of Transcription Factors in Carcinogenesis.International journal of molecular sciences · 2021Review
- MOF upregulates the estrogen receptor α signaling pathway by its acetylase activity in hepatocellular carcinoma.Cancer science · 2021Article
- The Biological Significance of Targeting Acetylation-Mediated Gene Regulation for Designing New Mechanistic Tools and Potential Therapeutics.Biomolecules · 2021Review
- Post-Translational Modifications That Drive Prostate Cancer Progression.Biomolecules · 2021Review
- Lack of MOF Decreases Susceptibility to Hypoxia and Promotes Multidrug Resistance in Hepatocellular Carcinoma via HIF-1α.Frontiers in cell and developmental biology · 2021Article
- Epigenetic activation of the small GTPase TCL contributes to colorectal cancer cell migration and invasion.Oncogenesis · 2020Article
- TNF-α regulates diabetic macrophage function through the histone acetyltransferase MOF.JCI insight · 2020Article
- The Versatility of Sirtuin-1 in Endocrinology and Immunology.Frontiers in cell and developmental biology · 2020Review
- MYST1/KAT8 contributes to tumor progression by activating EGFR signaling in glioblastoma cells.Cancer medicine · 2019Article
- Exploiting Epigenetic Alterations in Prostate Cancer.International journal of molecular sciences · 2017Review
Corrections and comments
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Authors and funding
10 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In prostate cancer (PCa), the functional synergy between androgen receptor (AR) and nuclear factor-κ B (NF-κB) escalates the resistance to therapeutic regimens and promotes aggressive tumor growth. Although the underlying mechanisms are less clear, gene regulatory abilities of coactivators can bridge the transcription functions of AR and NF-κB. The present study shows that MYST1 (MOZ, YBF2 and SAS2, and TIP60 protein 1) costimulates AR and NF-κB functions in PCa cells. We demonstrate that activation of NF-κB promotes deacetylation of MYST1 by sirtuin 1. Further, the mutually exclusive interactions of MYST1 with sirtuin 1 vs AR regulate the acetylation of lysine 16 on histone H4. Notably, in AR-lacking PC3 cells and in AR-depleted LNCaP cells, diminution of MYST1 activates the cleavage of poly(ADP-ribose) polymerase and caspase 3 that leads to apoptosis. In contrast, in AR-transformed PC3 cells (PC3-AR), depletion of MYST1 induces cyclin-dependent kinase (CDK) N1A/p21, which results in G2M arrest. Concomitantly, the levels of phospho-retinoblastoma, E2F1, CDK4, and CDK6 are reduced. Finally, the expression of tumor protein D52 (TPD52) was unequivocally affected in PC3, PC3-AR, and LNCaP cells. Taken together, the results of this study reveal that the functional interactions of MYST1 with AR and NF-κB are critical for PCa progression.
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