ArticleJournal of pharmaceutical analysis2023
Epigenetic drug library screening reveals targeting DOT1L abrogates NAD
Article in Journal of pharmaceutical analysis, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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
9 citing papers in PubMed, 13 citations in OpenAlex.
- Extracellular Matrix Stiffness Regulates Cancer Stemness in Uveal Melanoma via the PIEZO1-DOT1L Axis.Investigative ophthalmology & visual science · 2025Article
- Targeted reduction-responsive nanovehicles for photodynamic therapy-primed immunotherapy in melanoma.Journal of pharmaceutical analysis · 2025Article
- SETDB1 is critically required for uveal melanoma growth and represents a promising therapeutic target.Cell death & disease · 2025Article
- RBM30 recruits DOT1L to activate STAT1 transcription and drive immune evasion in hepatocellular carcinoma.Oncogene · 2025Article
- Super-enhancers orchestrate transcriptional dysregulation and metabolic reprogramming in uveal melanoma.Communications biology · 2025Article
- Cut&tag: a powerful epigenetic tool for chromatin profiling.Epigenetics · 2024Review
- Targeting the chromatin structural changes of antitumor immunity.Journal of pharmaceutical analysis · 2024Review
- Inhibitors of NADInternational journal of molecular sciences · 2024Review
- Targeting histone deacetylase suppresses tumor growth through eliciting METTL14-modified mCancer communications (London, England) · 2023Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Uveal melanoma (UM) is the most frequent and life-threatening ocular malignancy in adults. Aberrant histone methylation contributes to the abnormal transcriptome during oncogenesis. However, a comprehensive understanding of histone methylation patterns and their therapeutic potential in UM remains enigmatic. Herein, using a systematic epi-drug screening and a high-throughput transcriptome profiling of histone methylation modifiers, we observed that disruptor of telomeric silencing-1-like (DOT1L), a methyltransferase of histone H3 lysine 79 (H3K79), was activated in UM, especially in the high-risk group. Concordantly, a systematic epi-drug library screening revealed that DOT1L inhibitors exhibited salient tumor-selective inhibitory effects on UM cells, both in vitro and in vivo. Combining Cleavage Under Targets and Tagmentation (CUT&Tag), RNA sequencing (RNA-seq), and bioinformatics analysis, we identified that DOT1L facilitated H3K79 methylation of nicotinate phosphoribosyltransferase (NAPRT) and epigenetically activated its expression. Importantly, NAPRT served as an oncogenic accelerator by enhancing nicotinamide adenine dinucleotide (NAD
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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.