ReviewBiochemical Society transactions2016
Targeting cancer using KAT inhibitors to mimic lethal knockouts.
Review in Biochemical Society transactions, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
40 citing papers in PubMed, 72 citations in OpenAlex.
- Mitigation of Injury from Myocardial Infarction by Pentamidine, an Inhibitor of the Acetyltransferase Tip60.Cardiovascular drugs and therapy · 2026Article
- Arginine methylation in cancer: mechanisms and therapeutic implications.Biomarker research · 2025Review
- Histone Deacetylases (HDACs) Roles in Inflammation-mediated Diseases; Current Knowledge.Cell biochemistry and biophysics · 2025Review
- KAT5 regulates neurodevelopmental states associated with G0-like populations in glioblastoma.Nature communications · 2025Article
- Review
- Current trends in clinical trials and the development of small molecule epigenetic inhibitors as cancer therapeutics.Epigenomics · 2024Review
- Prediction of Distant Metastases in Patients with Kidney Cancer Based on Gene Expression and Methylation Analysis.Diagnostics (Basel, Switzerland) · 2023Article
- Expression profiles and functional prediction of histone acetyltransferases of the MYST family in kidney renal clear cell carcinoma.BMC cancer · 2023Article
- TIP60 is required for tumorigenesis in non-small cell lung cancer.Cancer science · 2023Article
- Pharmacological inhibition of the acetyltransferase Tip60 mitigates myocardial infarction injury.Disease models & mechanisms · 2023Article
- The roles of histone modifications in tumorigenesis and associated inhibitors in cancer therapy.Journal of the National Cancer Center · 2022Review
- Targeting Histone Epigenetic Modifications and DNA Damage Responses in Synthetic Lethality Strategies in Cancer?Cancers · 2022Article
- Article
- Recurrent chromosomal translocations in sarcomas create a megacomplex that mislocalizes NuA4/TIP60 to Polycomb target loci.Genes & development · 2022Article
- Article
- Transcriptomic and genomic studies classify NKL54 as a histone deacetylase inhibitor with indirect influence on MEF2-dependent transcription.Nucleic acids research · 2022Article
- Aspirin Suppressed PD-L1 Expression through Suppressing KAT5 and Subsequently Inhibited PD-1 and PD-L1 Signaling to Attenuate OC Development.Journal of oncology · 2022Article
- Editorial: Mechanisms guarding the genome.Frontiers in cell and developmental biology · 2022Article
- Histone modification and histone modification-targeted anti-cancer drugs in breast cancer: Fundamentals and beyond.Frontiers in pharmacology · 2022Review
- KAT5 histone acetyltransferase mutations in cancer cells.microPublication biology · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Two opposing enzyme classes regulate fundamental elements of genome maintenance, gene regulation and metabolism, either through addition of an acetyl moiety by histone acetyltransferases (HATs) or its removal by histone de-acetyltransferases (HDAC), and are exciting targets for drug development. Importantly, dysfunctional acetylation has been implicated in numerous diseases, including cancer. Within the HAT superfamily the MYST family holds particular interest, as its members are directly involved in the DNA damage response and repair pathways and crucially, several members have been shown to be down-regulated in common cancers (such as breast and prostate). In the present study we focus on the development of lysine (K) acetyltransferase inhibitors (KATi) targeting the MYST family member Tip60 (Kat5), an essential protein, designed or discovered through screening libraries. Importantly, Tip60 has been demonstrated to be significantly down-regulated in many cancers which urgently require new treatment options. We highlight current and future efforts employing these KATi as cancer treatments and their ability to synergize and enhance current cancer treatments. We investigate the different methods of KATi production or discovery, their mechanisms and their validation models. Importantly, the utility of KATi is based on a key concept: using KATi to abrogate the activity of an already down-regulated essential protein (effectively creating a lethal knockout) provides another innovative mechanism for targeting cancer cells, while significantly minimizing any off-target effects to normal cells. This approach, combined with the rapidly developing interest in KATi, suggests that KATi have a bright future for providing truly personalized therapies.
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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.