ReviewInternational journal of molecular sciences2022
Interplay between A-to-I Editing and Splicing of RNA: A Potential Point of Application for Cancer Therapy.
Review in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
13 citing papers in PubMed, 40 citations in OpenAlex.
- Targeting ADAR1 in Cancer: Biology, Therapeutic Strategies, Challenges, and Limitations.Pharmaceuticals (Basel, Switzerland) · 2026Review
- RNA editing: an emerging frontier in cancer therapy - explorations, opportunities, and challenges.International journal of surgery (London, England) · 2026Article
- The context-dependent role of the dsRNA response in linking A-to-I editing and ADAR to normal hematopoiesis and leukemia.Frontiers in cell and developmental biology · 2026Review
- Review
- Unraveling ADAR-Mediated Protein Recoding: A Proteogenomic Exploration in Model Organisms and Human Pathology.International journal of molecular sciences · 2025Review
- Immunomodulatory role of RNA modifications in sex hormone-dependent cancers.Frontiers in immunology · 2025Review
- Comprehensive analysis of the relationship between RNA modification writers and immune microenvironment in head and neck squamous cell carcinoma.BMC immunology · 2024Article
- Dysregulated RNA editing of EIF2AK2 in polycystic ovary syndrome: clinical relevance and functional implications.BMC medicine · 2024Article
- RNA editing enzymes: structure, biological functions and applications.Cell & bioscience · 2024Review
- Identification of prognostic RNA editing profiles for clear cell renal carcinoma.Frontiers in medicine · 2024Article
- Harnessing ADAR-Mediated Site-Specific RNA Editing in Immune-Related Disease: Prediction and Therapeutic Implications.International journal of molecular sciences · 2023Review
- Lactobacillus for ribosome peptide editing cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023Review
- RNA Modifications Meet Tumors.Cancer management and research · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Adenosine-to-inosine RNA editing is a system of post-transcriptional modification widely distributed in metazoans which is catalyzed by ADAR enzymes and occurs mostly in double-stranded RNA (dsRNA) before splicing. This type of RNA editing changes the genetic code, as inosine generally pairs with cytosine in contrast to adenosine, and this expectably modulates RNA splicing. We review the interconnections between RNA editing and splicing in the context of human cancer. The editing of transcripts may have various effects on splicing, and resultant alternatively spliced isoforms may be either tumor-suppressive or oncogenic. Dysregulated RNA splicing in cancer often causes the release of excess amounts of dsRNA into cytosol, where specific dsRNA sensors provoke antiviral-like responses, including type I interferon signaling. These responses may arrest cell division, causing apoptosis and, externally, stimulate antitumor immunity. Thus, small-molecule spliceosome inhibitors have been shown to facilitate the antiviral-like signaling and are considered to be potential cancer therapies. In turn, a cytoplasmic isoform of ADAR can deaminate dsRNA in cytosol, thereby decreasing its levels and diminishing antitumor innate immunity. We propose that complete or partial inhibition of ADAR may enhance the proapoptotic and cytotoxic effects of splicing inhibitors and that it may be considered a promising addition to cancer therapies targeting RNA splicing.
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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.