ArticleGenome medicine2015
The oxidative demethylase ALKBH3 marks hyperactive gene promoters in human cancer cells.
Article in Genome medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 26 citations in OpenAlex.
- ALKBH3 m1A Demethylase Deficiency Reduces Alzheimer's Amyloid-β Pathology.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Transcriptomic Insights into Late-Life Depression and the Role of Environmental Drinking Water Composition: A Study on 18-Month-Old Mice.International journal of molecular sciences · 2025Article
- Biological interpretation of DNA/RNA modification by ALKBH proteins and their role in human cancer.European journal of medical research · 2025Review
- Genetic and Epigenetic Biomarkers Associated with Early Relapse in Pediatric Acute Lymphoblastic Leukemia: A Focused Bioinformatics Study on DNA-Repair Genes.Biomedicines · 2024Article
- Rare variant analyses validate known ALS genes in a multi-ethnic population and identifies ANTXR2 as a candidate in PLS.BMC genomics · 2024Article
- Phylogenetic and functional analyses ofmSphere · 2024Article
- Rare variant analyses validate known ALS genes in a multi-ethnic population and identifiesResearch square · 2023Article
- Engineering diabetic human skin equivalent forFrontiers in bioengineering and biotechnology · 2022Article
- Roles of RNA Modifications in Diverse Cellular Functions.Frontiers in cell and developmental biology · 2022Review
- Interleukin-17 receptor D (Sef) is a multi-functional regulator of cell signaling.Cell communication and signaling : CCS · 2021Review
- Multi-substrate selectivity based on key loops and non-homologous domains: new insight into ALKBH family.Cellular and molecular life sciences : CMLS · 2021Review
- OTUD4 Is a Phospho-Activated K63 Deubiquitinase that Regulates MyD88-Dependent Signaling.Molecular cell · 2018Article
- AlkB homolog 3-mediated tRNA demethylation promotes protein synthesis in cancer cells.Scientific reports · 2017Article
- Genome-Wide Association Study for Carcass Traits in an Experimental Nelore Cattle Population.PloS one · 2017Article
- Rhein Inhibits AlkB Repair Enzymes and Sensitizes Cells to Methylated DNA Damage.The Journal of biological chemistry · 2016Article
- Epigenetics of Aging and Alzheimer's Disease: Implications for Pharmacogenomics and Drug Response.International journal of molecular sciences · 2015Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe oxidative DNA demethylase ALKBH3 targets single-stranded DNA (ssDNA) in order to perform DNA alkylation damage repair. ALKBH3 becomes upregulated during tumorigenesis and is necessary for proliferation. However, the underlying molecular mechanism remains to be understood.
methodsTo further elucidate the function of ALKBH3 in cancer, we performed ChIP-seq to investigate the genomic binding pattern of endogenous ALKBH3 in PC3 prostate cancer cells coupled with microarray experiments to examine the expression effects of ALKBH3 depletion.
resultsWe demonstrate that ALKBH3 binds to transcription associated locations, such as places of promoter-proximal paused RNA polymerase II and enhancers. Strikingly, ALKBH3 strongly binds to the transcription initiation sites of a small number of highly active gene promoters. These promoters are characterized by high levels of transcriptional regulators, including transcription factors, the Mediator complex, cohesin, histone modifiers, and active histone marks. Gene expression analysis showed that ALKBH3 does not directly influence the transcription of its target genes, but its depletion induces an upregulation of ALKBH3 non-bound inflammatory genes.
conclusionsThe genomic binding pattern of ALKBH3 revealed a putative novel hyperactive promoter type. Further, we propose that ALKBH3 is an intrinsic DNA repair protein that suppresses transcription associated DNA damage at highly expressed genes and thereby plays a role to maintain genomic integrity in ALKBH3-overexpressing cancer cells. These results raise the possibility that ALKBH3 may be a potential target for inhibiting cancer progression.
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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.