ADARB1 (Adenosine Deaminase RNA Specific B1)

ADARB1 exerts its anti-tumor effects primarily through the HMGB1/PFKFB3 pathway. Collectively, these findings identify ADARB1 as a novel tumor suppressor in cervical cancer and a promising therapeutic target for clinical intervention.

This study underscores the biological relevance of RNA editing in CRC, highlighting its impact on chemoresistance, the tumor microenvironment, and subtype-specific gene regulation. Our findings suggest that RNA editing represents a critical post-transcriptional regulatory layer in CRC and holds potential as a biomarker and therapeutic target.

While some alternative splicing-regulatory roles of inosine and ADAR enzymes are established, we observe that altering ADAR2 and ADAR1/ADAR2 is associated with changes in alternative splicing and coincides with shifts in levels of other RNA modification. Through the utilization of an innovative approach, we identified novel candidate circular RNA profiles in wild-type and mutant mice and detected potential inosine sites within circular RNAs. Collectively, our findings underscore a complex interplay among RNA modifications, alternative splicing, circular RNAs in the mouse brain.

High ADARB2 expression was associated with markedly improved overall survival, whereas low expression correlated with enrichment of oncogenic pathways, including Wnt/β-catenin, Notch, and Hedgehog, consistent with a poorer clinical prognosis. These findings highlight ADARB2 as a promising diagnostic biomarker and independent prognostic factor in HNSCC.

The A-to-I RNA edited miR-605-3p demonstrates a more potent anti-tumor effect in CRC by modulating CD8+ T cell immune infiltration mediated by CDK6. This study unveils edited miR-605-3p as a potential prognostic biomarker and highlights the ADAR2-miR-605-3p axis as a novel therapeutic target for CRC.

Moreover, we highlight the potential of ADARs as prognostic biomarkers and promising therapeutic targets in oncology. This review aims to spark novel precision oncology and cancer immunotherapy strategies by bridging molecular insights with translational applications.

Finally, MFN1 editing correlated with prolonged time to treatment and overall survival in CLL patients. Summarizing, we identified a novel ADARB1 function as C to U editing regulator, which regulates MFN1 splicing and MFN1 S329L recoding with pathogenic relevance in CLL.

Using RNA pull-down and mass spectrometry, we discovered that circADARB1 facilitates the interaction of YBX1 protein with m6A-modified ZEB1 mRNA, thereby stabilizing ZEB1 mRNA and upregulating ZEB1 expression. This study uncovers a novel role of circADARB1 in NPC progression and identifies YBX1 as a potential m6A reader, offering new potential molecular markers and therapeutic targets for NPC.

Drosophila lacks an ADAR1 homolog; instead, the ADAR2 homolog is responsible for editing double-stranded RNA to prevent aberrant activation of the innate immune system. Finally, we address major questions in the field that still remain unanswered.

Ed-miR-3167 exerted tumor inhibitory effect in LUAD by weakening the carcinogenesis of SSR2. A-to-I RNA edited miR-3167 curbs malignant behaviors of LUAD by activating Hippo signaling through downregulating SSR2, indicating that edited miR-3167 has the potential as a therapeutic target for LUAD.

Additionally, five high-quality full-length ADAR2 models were developed. These models provide insights into ADAR2 function, mutation impacts, and potential areas for protein engineering to enhance stability, RNA-binding specificity, or protein interactions, particularly concerning dimerization or complex formation with other proteins and RNAs.

Our findings highlight the role of AR in the response to BCG therapy by modulating PD-L1 expression and TILs through the ADAR2, miR-200a-3p, and INF-γ pathways. Furthermore, our data provides valuable insights for optimizing BCG therapy in patients with CIS, paving the way for other possible combined treatment strategies.