Fig. 3

Regulatory mechanisms of A-to-I editing in miRNAs and mRNAs. ADAR2 can promote CD97-mediated apoptosis by modifying miR-379-5p, leading to antioncogenic effects. Additionally, ADAR enzymes compete with Drosha for binding to pri-miRNAs, inhibiting their processing into pre-miRNAs. This inhibition enhances tumor cell proliferation, invasion, and metastasis. MicroRNAs typically function by binding to mRNAs to inhibit translation or promote degradation, thereby reducing the levels of target proteins. However, ADAR-mediated modifications of miRNAs (such as miR-3144-3p and miR-200b) or mRNAs (such as EMP2, MTTL3, and MSI2) can disrupt these interactions, allowing for the uninterrupted translation of oncogenic mRNAs. This process ultimately leads to increased tumor cell proliferation and invasion. Moreover, ADAR1 can dimerize with Dicer to enhance the modification and processing of oncogenic miRNAs, promoting epithelial-mesenchymal transition (EMT) and accelerating tumor progression