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AZIN1 RNA editing alters protein interactions, leading to nuclear translocation and worse outcomes in prostate cancer. | LitMetric

AI Article Synopsis

  • * edAZIN1 binds to actin and myosin proteins, allowing it to move into the nucleus, while the unedited version (wtAZIN1) does not promote this behavior, resulting in different cellular effects related to cancer aggressiveness.
  • * In prostate cancer patients, the presence of edited AZIN1 and its nuclear localization correlate with poorer outcomes, including higher Gleason scores, greater genomic instability, and shorter progression-free survival periods.

Article 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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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9636422PMC
http://dx.doi.org/10.1038/s12276-022-00845-6DOI Listing

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