ArticleMolecular therapy : the journal of the American Society of Gene Therapy2021
Targeting RNA editing of antizyme inhibitor 1: A potential oligonucleotide-based antisense therapy for cancer.
Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 34 citations in OpenAlex.
- ADAR1 regulates radiosensitivity in ESCC through cIAP2-NF-κB signaling and C16orf46 editing.iScience · 2026Article
- Targeting ADAR1 in Cancer: Biology, Therapeutic Strategies, Challenges, and Limitations.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Review
- A-to-I edited SNHG3 promotes non-small cell lung cancer metastasis by promoting fatty acid oxidation and resisting ferroptosis.Communications biology · 2025Article
- SNORA74A Drives Self-Renewal of Liver Cancer Stem Cells and Hepatocarcinogenesis Through Activation of Notch3 Signaling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Biochemical profiling and structural basis of ADAR1-mediated RNA editing.Molecular cell · 2025Article
- The roles and mechanisms of coding and noncoding RNA variations in cancer.Experimental & molecular medicine · 2024Review
- Targeting and engineering long non-coding RNAs for cancer therapy.Nature reviews. Genetics · 2024Review
- Reovirus infection induces transcriptome-wide unique A-to-I editing changes in the murine fibroblasts.Virus research · 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
- Suppression of A-to-I RNA-editing enzyme ADAR1 sensitizes hepatocellular carcinoma cells to oxidative stress through regulating Keap1/Nrf2 pathway.Experimental hematology & oncology · 2024Article
- Antizyme inhibitor family: biological and translational research implications.Cell communication and signaling : CCS · 2024Review
- MALAT1/ mir-1-3p mediated BRF2 expression promotes HCC progression via inhibiting the LKB1/AMPK signaling pathway.Cancer cell international · 2023Article
- RNA editing of AZIN1 coding sites is catalyzed by ADAR1 p150 after splicing.The Journal of biological chemistry · 2023Article
- Epigenetic regulation in the tumor microenvironment: molecular mechanisms and therapeutic targets.Signal transduction and targeted therapy · 2023Review
- Molecular Docking and Dynamics Simulation Studies Predict Potential Anti-ADAR2 Inhibitors: Implications for the Treatment of Cancer, Neurological, Immunological and Infectious Diseases.International journal of molecular sciences · 2023Article
- Recent Advances in Adenosine-to-Inosine RNA Editing in Cancer.Cancer treatment and research · 2023Review
- ADAR1 and its implications in cancer development and treatment.Trends in genetics : TIG · 2022Review
- The development and improvement of ribonucleic acid therapy strategies.Molecular therapy. Nucleic acids · 2021Review
Corrections and comments
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Authors and funding
23 authors at 6 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dysregulated adenosine-to-inosine (A-to-I) RNA editing is implicated in various cancers. However, no available RNA editing inhibitors have so far been developed to inhibit cancer-associated RNA editing events. Here, we decipher the RNA secondary structure of antizyme inhibitor 1 (AZIN1), one of the best-studied A-to-I editing targets in cancer, by locating its editing site complementary sequence (ECS) at the 3' end of exon 12. Chemically modified antisense oligonucleotides (ASOs) that target the editing region of AZIN1 caused a substantial exon 11 skipping, whereas ECS-targeting ASOs effectively abolished AZIN1 editing without affecting splicing and translation. We demonstrate that complete 2'-O-methyl (2'-O-Me) sugar ring modification in combination with partial phosphorothioate (PS) backbone modification may be an optimal chemistry for editing inhibition. ASO3.2, which targets the ECS, specifically inhibits cancer cell viability in vitro and tumor incidence and growth in xenograft models. Our results demonstrate that this AZIN1-targeting, ASO-based therapeutics may be applicable to a wide range of tumor types.
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Registered trials
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