ReviewOncogene2015
KATs in cancer: functions and therapies.
Review in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
70 citing papers in PubMed, 131 citations in OpenAlex.
- O-GlcNAcylation of KAT2A Enhances Bladder Cancer Proliferation by Inhibiting the KAT2A-TRIM22 Interaction.Cancer science · 2026Article
- Multiple Regulatory Mechanisms of Post-Translational Modifications and Therapeutic Potential of Mitotic Catastrophe.International journal of molecular sciences · 2026Review
- Dual Regulation of Post-Translational Modification of Proteins: Bottlenecks and Breakthroughs in NK Cell Therapy for Glioblastoma.International journal of general medicine · 2026Review
- Lysine Acetyltransferase 6 in Health and Disease.MedComm · 2025Review
- Crosstalk between acetylation modification and autophagy in cancer: roles, mechanisms, and therapeutic potential.Cell death discovery · 2025Review
- Lysine Acetyltransferase 6 Complexes in Neurodevelopmental Disorders and Different Types of Cancer.Results and problems in cell differentiation · 2025Review
- The role of acetylation and deacetylation in cancer metabolism.Clinical and translational medicine · 2025Review
- A novel histone acetylation-associated gene signature with prognostic value in Ewing sarcoma.Discover oncology · 2024Article
- Identification of ETV5 as a prognostic marker related to epigenetic modification in pan-cancer and facilitates tumor progression in hepatocellular carcinoma.Scientific reports · 2024Article
- Role of the CTCF/p300 axis in osteochondrogenic-like differentiation of polyploid giant cancer cells with daughter cells.Cell communication and signaling : CCS · 2024Article
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- KAT8 compound inhibition inhibits the initial steps of PINK1-dependant mitophagy.Scientific reports · 2024Article
- Paralogue-selective degradation of the lysine acetyltransferase EP300.bioRxiv : the preprint server for biology · 2024Article
- Discovery and Characterization of Active CBP/EP300 Degraders Targeting the HAT Domain.ACS medicinal chemistry letters · 2024Article
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- Comparative Analysis of Drug-like EP300/CREBBP Acetyltransferase Inhibitors.ACS chemical biology · 2023Article
- Comparative analysis of drug-like EP300/CREBBP acetyltransferase inhibitors.bioRxiv : the preprint server for biology · 2023Article
10 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Post-translational acetylation of lysines is most extensively studied in histones, but this modification is also found in many other proteins and is implicated in a wide range of biological processes in both the cell nucleus and the cytoplasm. Like phosphorylation, acetylation patterns and levels are often altered in cancer, therefore small molecule inhibition of enzymes that regulate acetylation and deacetylation offers much potential for inhibiting cancer cell growth, as does disruption of interactions between acetylated residues and 'reader' proteins. For more than a decade now, histone deacetylase inhibitors have been investigated for their ability to increase acetylation and promote expression of tumor suppressor genes. However, emerging evidence suggests that acetylation can also promote cancer, in part by enhancing the functions of oncogenic transcription factors. In this review, we focus on how acetylation of both histone and non-histone proteins may drive cancer, and we will discuss the implications of such changes on how patients are assigned to therapeutic agents. Finally, we will explore what the future holds in the design of small-molecule inhibitors for modulation of levels or functions of acetylation states.
Indexed as
Identifiers
What OpenQuestion holds
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.