ArticleCancer research communications2021
8-azaadenosine and 8-chloroadenosine are not selective inhibitors of ADAR.
Article in Cancer research communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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
23 citing papers in PubMed, 35 citations in OpenAlex.
- Targeting ADAR1 in Cancer: Biology, Therapeutic Strategies, Challenges, and Limitations.Pharmaceuticals (Basel, Switzerland) · 2026Review
- All-trans retinoic acid destabilizes ADAR1 protein through retinoylation-mediated USP7 dissociation and improves immunotherapy in pancreatic cancer.Nature communications · 2026Article
- Targeting RNA binding proteins with small-molecule inhibitors: Advances, challenges, and therapeutic opportunities.Acta pharmaceutica Sinica. B · 2026Review
- Identification of ADAR1i-124: The first effective A-to-I RNA editing inhibitor with promising cancer therapeutic potential.iScience · 2026Article
- Deaminase Modulation Driving a New Era in Drug Development.International journal of molecular sciences · 2025Review
- ZYS-1 is not an ADAR1 inhibitor.RNA (New York, N.Y.) · 2025Article
- ADAR1-mediated RNA editing in breast cancer: molecular mechanisms and therapeutic implications.Medical oncology (Northwood, London, England) · 2025Review
- Autocrine interferon poisoning mediates ADAR1-dependent synthetic lethality in BRCA1/2-mutant cancers.Nature communications · 2025Article
- Engineering circular guide RNA and CRISPR-Cas13d-encoding mRNA for the RNA editing ofbioRxiv : the preprint server for biology · 2025Article
- ADAR1-high tumor-associated macrophages induce drug resistance and are therapeutic targets in colorectal cancer.Molecular cancer · 2025Article
- Article
- Immunomodulatory role of RNA modifications in sex hormone-dependent cancers.Frontiers in immunology · 2025Review
- Suppression of double-stranded RNA sensing in cancer: molecular mechanisms and therapeutic potential.Biochemical Society transactions · 2024Review
- Nuclear aggregates of NONO/SFPQ and A-to-I-edited RNA in Parkinson's disease and dementia with Lewy bodies.Neuron · 2024Article
- ADAR-Mediated A>I(G) RNA Editing in the Genotoxic Drug Response of Breast Cancer.International journal of molecular sciences · 2024Review
- Structural and functional effects of inosine modification in mRNA.RNA (New York, N.Y.) · 2024Article
- Induction of Viral Mimicry Upon Loss of DHX9 and ADAR1 in Breast Cancer Cells.Cancer research communications · 2024Article
- Structurally Specific Z-DNA Proteolysis Targeting Chimera Enables Targeted Degradation of Adenosine Deaminase Acting on RNA 1.Journal of the American Chemical Society · 2024Article
- Induction of viral mimicry upon loss of DHX9 and ADAR1 in breast cancer cells.bioRxiv : the preprint server for biology · 2023Article
- A-to-I RNA editing by ADAR and its therapeutic applications: From viral infections to cancer immunotherapy.Wiley interdisciplinary reviews. RNA · 2023Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The RNA editing enzyme ADAR, is an attractive therapeutic target for multiple cancers. Through its deaminase activity, ADAR edits adenosine to inosine in dsRNAs. Loss of ADAR in some cancer cell lines causes activation of the type I interferon pathway and the PKR translational repressor, leading to inhibition of proliferation and stimulation of cell death. As such, inhibition of ADAR function is a viable therapeutic strategy for many cancers. However, there are no FDA approved inhibitors of ADAR. Two small molecules have been previously shown to inhibit ADAR or reduce its expression: 8-azaadenosine and 8-chloroadenosine. Here we show that neither molecule is a selective inhibitor of ADAR. Both 8-azaadenosine and 8-chloroadenosine show similar toxicity to ADAR-dependent and independent cancer cell lines. Furthermore, the toxicity of both small molecules is comparable between cell lines with either knockdown or overexpression of ADAR, and cells with unperturbed ADAR expression. Treatment with neither molecule causes activation of PKR. Finally, treatment with either molecule has no effect on A-to-I editing of multiple ADAR substrates. Together these data show that 8-azaadenosine and 8-chloroadenosine are not suitable small molecules for therapies that require selective inhibition of ADAR, and neither should be used in preclinical studies as ADAR inhibitors.
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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.