ArticleExperimental & molecular medicine2022
AZIN1 RNA editing alters protein interactions, leading to nuclear translocation and worse outcomes in prostate cancer.
Article in Experimental & molecular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 13 citations in OpenAlex.
- The regulatory mechanism and clinical significance of RNA editing in prostate cancer.Current urology · 2026Review
- Molecular Mechanisms of Sepsis-Associated Acute Kidney Injury.Journal of the American Society of Nephrology : JASN · 2025Review
- [ADAR1 Regulates the ERK/c-FOS/MMP-9 Pathway to Drive the Proliferation and Migration of Non-small Cell Lung Cancer Cells].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2025Article
- RNA modifications in the tumor microenvironment: insights into the cancer-immunity cycle and beyond.Experimental hematology & oncology · 2025Review
- AZIN1 level is increased in medulloblastoma and correlates with c-Myc activity and tumor phenotype.Journal of experimental & clinical cancer research : CR · 2025Article
- Inflammation primes the murine kidney for recovery by activating AZIN1 adenosine-to-inosine editing.The Journal of clinical investigation · 2024Article
- Reovirus infection induces transcriptome-wide unique A-to-I editing changes in the murine fibroblasts.Virus research · 2024Article
- Review
- The role of ADAR1 through and beyond its editing activity in cancer.Cell communication and signaling : CCS · 2024Review
- Antizyme inhibitor family: biological and translational research implications.Cell communication and signaling : CCS · 2024Review
- Inflammation primes the kidney for recovery by activating AZIN1 A-to-I editing.bioRxiv : the preprint server for biology · 2023Article
Corrections and comments
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Authors and funding
8 authors at 5 institutions in 2 countries.
Funding
Abstract
The transcript encoding Antizyme Inhibitor 1 (AZIN1) is frequently edited in various cancers, and this editing is associated with enhanced tumor aggressiveness. After comparison of wild-type AZIN1 (wtAZIN1) and edited AZIN1 (edAZIN1, which contains a Ser367Gly substitution), we report differential binding of edAZIN1 to a small set of proteins; specifically, edAZIN1 binds to alpha-smooth muscle actin (ACTA2), gamma actin 1 (ACTG1), and myosin9, whereas wtAZIN1 does not. This binding enables nuclear translocation of edAZIN1. In contrast to overexpression of edAZIN1 and, to a lesser extent, (editable) wtAZIN1, overexpression of an uneditable AZIN1 allele does not promote a cellular phenotype associated with increased tumorigenicity. In patients, both editing and nuclear localization of AZIN1 are common and are associated with tumor aggressiveness, i.e., a higher Gleason score, higher genomic instability, and a shorter progression-free survival time. In conclusion, the data indicate that binding of edAZIN1 to the actin/myosin9 complex supports its nuclear translocation, leading to enhanced cellular aggressiveness, and is associated with worse prostate cancer outcomes.
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