Riox2, also known as ribosomal oxygenase 2, MINA53, and mdig, is a member of the JmjC family proteins. It functions as a histone demethylase and ribosomal oxygenase, modifying ribosomal proteins by histidine hydroxylation. It has been implicated in regulating chromatin-based processes and transcription, and is associated with cell proliferation pathways. Understanding Riox2's function is crucial as it is involved in various biological processes and diseases [4,5,6].

In prostate cancers, Riox2 is overexpressed and is an independent prognostic factor for disease-specific survival, being associated with late-stage diseases, adverse Gleason scores, TP53 gene mutation, and disease-free status. Its upregulation may be due to c-Myc upregulation, and in castration-resistant prostate cancers, its expression is positively correlated with AR signaling index but negatively correlated with the neuroendocrinal progression index [1]. In lung adenocarcinoma and squamous cell carcinoma, Riox2 is highly expressed, and its expression is negatively correlated with its methylation level at specific CpG sites, although it may not be an independent prognostic biomarker [2]. In renal cell tumors, Riox2 is differentially expressed, with higher levels in cases that developed metastasis during follow-up in a cohort of clear cell renal cell carcinoma, suggesting its involvement in renal tumorigenesis and RCC progression, especially in metastatic spread [3].

In conclusion, Riox2 plays significant roles in multiple cancer-related biological processes. Model-based research, especially in the context of these cancers, reveals that Riox2 is involved in tumor progression, prognosis, and potentially in metastasis. Understanding Riox2 through gene knockout or conditional knockout models could potentially offer insights into novel therapeutic strategies for these diseases.