ArticleCancers2022
CREPT Disarms the Inhibitory Activity of HDAC1 on Oncogene Expression to Promote Tumorigenesis.
Article in Cancers, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed, 6 citations in OpenAlex.
- From Environmental Exposure to Intervertebral Disc Degeneration: First Evidence of Pro-Degenerative Effects of Polyamide 6 Microplastics.Biomedicines · 2026Article
- Targeted suppression of tumor growth by CREPT promoter-driven diphtheria toxin fragment A.Cancer gene therapy · 2026Article
- A histone acetylation score for prognostic stratification and immunogenomic profiling in esophageal cancer.Discover oncology · 2025Article
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
Histone deacetylases 1 (HDAC1), an enzyme that functions to remove acetyl molecules from ε-NH3 groups of lysine in histones, eliminates the histone acetylation at the promoter regions of tumor suppressor genes to block their expression during tumorigenesis. However, it remains unclear why HDAC1 fails to impair oncogene expression. Here we report that HDAC1 is unable to occupy at the promoters of oncogenes but maintains its occupancy with the tumor suppressors due to its interaction with CREPT (cell cycle-related and expression-elevated protein in tumor, also named RPRD1B), an oncoprotein highly expressed in tumors. We observed that CREPT competed with HDAC1 for binding to oncogene (such as
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Registered trials
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