Fig. 2
A-to-I editing in mRNA coding region resulting in missense mutation. When A-to-I editing occurs, as seen in AZIN1, it leads to non-synonymous mutations that promote tumor growth. This mutation elevates IL-8 levels, driving angiogenesis, while also increasing the protein’s affinity for anti-enzymes, leading to their degradation and supporting tumor proliferation, invasion, and metastasis. Similarly, A-to-I editing in the coding regions of other mRNAs, such as FLNB, CDK13, RHOA, and KPC1, causes inosine to be read as guanosine during translation. This substitution can result in changes to amino acid residues, potentially altering the structure and function of the proteins, thus facilitating tumor cell proliferation, invasion, and metastasis. Additionally, ADAR2-catalyzed A-to-I editing of COPA mRNA produces the COPAI164V variant, which promotes oncogenesis by inhibiting the PI3K/AKT/mTOR signaling pathway